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by Karam Soliman</h3></div><div class="js-work-strip profile--work_container" data-work-id="124950491"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950491/Involvement_of_AKT_PI3K_Pathway_in_Sanguinarine_s_Induced_Apoptosis_and_Cell_Cycle_Arrest_in_Triple_negative_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Involvement of AKT/PI3K Pathway in Sanguinarine’s Induced Apoptosis and Cell Cycle Arrest in Triple-negative Breast Cancer Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081022/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950491/Involvement_of_AKT_PI3K_Pathway_in_Sanguinarine_s_Induced_Apoptosis_and_Cell_Cycle_Arrest_in_Triple_negative_Breast_Cancer_Cells">Involvement of AKT/PI3K Pathway in Sanguinarine’s Induced Apoptosis and Cell Cycle Arrest in Triple-negative Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>Cancer Genomics - Proteomics</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background/Aim: Chemotherapy resistance in triple-negative breast cancer (TNBC) cells is well doc...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background/Aim: Chemotherapy resistance in triple-negative breast cancer (TNBC) cells is well documented. Therefore, it is necessary to develop safer and more effective therapeutic agents to enhance the outcomes of chemotherapeutic agents. The natural alkaloid sanguinarine (SANG) has demonstrated therapeutic synergy when coupled with chemotherapeutic agents. SANG can also induce cell cycle arrest and trigger apoptosis in various cancer cells. Materials and Methods: In this study, we investigated the molecular mechanism underlying SANG activity in MDA-MB-231 and MDA-MB-468 cells as two genetically different models of TNBC. We employed various assays including Alamar Blue to measure the effect of SANG on cell viability and proliferation rate, flow cytometry analysis to study the potential of the compound to induce apoptosis and cell cycle arrest, quantitative qRT PCR apoptosis array to measure the expression of different genes mediating apoptosis, and the western system was used to analyze the impact of the compound on AKT protein expression. Results: SANG lowered cell viability and disrupted cell cycle progression in both cell lines. Furthermore, S-phase cell cycle arrest-mediated apoptosis was found to be the primary contributor to cell growth inhibition in MDA-MB-231 cells. SANG-treated TNBC cells showed significantly up-regulated mRNA expression of 18 genes associated with apoptosis, including eight TNF receptor superfamily (TNFRSF), three members of the BCL2 family, and two members of the caspase (CASP) family in MDA-MB-468 cells. In MDA-MB-231 cells, two members of the TNF superfamily and four members of the BCL2 family were affected. The western study data showed the inhibition of AKT protein expression in both cell lines concurrent with up-regulated BCL2L11 gene. Our results point to the AKT/PI3K signaling pathway as one of the key mechanisms behind SANG-induced cell cycle arrest and death. Conclusion: SANG shows anticancer properties and apoptosis-related gene expression changes in the two TNBC cell lines and suggests AKT/PI3K pathway implication in apoptosis induction and cell cycle arrest. Thus, we propose SANG's potential as a solitary or supplementary treatment agent against TNBC. In the United States, breast cancer (BC) is the most common malignancy and the second leading cause of death among women aged 20-59 years (1). Gene expression is controlled by molecular signal transduction, and alterations in transcriptional settings distinguish cancer cells (2). BC is a heterogeneous cancer type categorized based on its molecular features. Triple-negative breast cancer (TNBC) affects approximately 15% of patients with BC (2). However, the incidence of this subtype is two to three folds higher in African American (AA) women than in other ethnic groups (3, 4). TNBC is the most aggressive BC and has a poor outcome compared to different BC subtypes (3, 5). Based on immunohistochemical characteristics, the expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) are missing in TNBC cells (3, 6). Currently, chemotherapy is the principal treatment for patients with TNBC. However, disease recurrence can manifest within the first two years 323</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="015425d7b9c904c13ed7c50f81785b85" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081022,"asset_id":124950491,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081022/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950491"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950491"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950491; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950491]").text(description); $(".js-view-count[data-work-id=124950491]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950491; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950491']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "015425d7b9c904c13ed7c50f81785b85" } } $('.js-work-strip[data-work-id=124950491]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950491,"title":"Involvement of AKT/PI3K Pathway in Sanguinarine’s Induced Apoptosis and Cell Cycle Arrest in Triple-negative Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Anticancer Research USA Inc.","grobid_abstract":"Background/Aim: Chemotherapy resistance in triple-negative breast cancer (TNBC) cells is well documented. Therefore, it is necessary to develop safer and more effective therapeutic agents to enhance the outcomes of chemotherapeutic agents. The natural alkaloid sanguinarine (SANG) has demonstrated therapeutic synergy when coupled with chemotherapeutic agents. SANG can also induce cell cycle arrest and trigger apoptosis in various cancer cells. Materials and Methods: In this study, we investigated the molecular mechanism underlying SANG activity in MDA-MB-231 and MDA-MB-468 cells as two genetically different models of TNBC. We employed various assays including Alamar Blue to measure the effect of SANG on cell viability and proliferation rate, flow cytometry analysis to study the potential of the compound to induce apoptosis and cell cycle arrest, quantitative qRT PCR apoptosis array to measure the expression of different genes mediating apoptosis, and the western system was used to analyze the impact of the compound on AKT protein expression. Results: SANG lowered cell viability and disrupted cell cycle progression in both cell lines. Furthermore, S-phase cell cycle arrest-mediated apoptosis was found to be the primary contributor to cell growth inhibition in MDA-MB-231 cells. SANG-treated TNBC cells showed significantly up-regulated mRNA expression of 18 genes associated with apoptosis, including eight TNF receptor superfamily (TNFRSF), three members of the BCL2 family, and two members of the caspase (CASP) family in MDA-MB-468 cells. In MDA-MB-231 cells, two members of the TNF superfamily and four members of the BCL2 family were affected. The western study data showed the inhibition of AKT protein expression in both cell lines concurrent with up-regulated BCL2L11 gene. Our results point to the AKT/PI3K signaling pathway as one of the key mechanisms behind SANG-induced cell cycle arrest and death. 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Based on immunohistochemical characteristics, the expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) are missing in TNBC cells (3, 6). Currently, chemotherapy is the principal treatment for patients with TNBC. 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Therefore, it is necessary to develop safer and more effective therapeutic agents to enhance the outcomes of chemotherapeutic agents. The natural alkaloid sanguinarine (SANG) has demonstrated therapeutic synergy when coupled with chemotherapeutic agents. SANG can also induce cell cycle arrest and trigger apoptosis in various cancer cells. Materials and Methods: In this study, we investigated the molecular mechanism underlying SANG activity in MDA-MB-231 and MDA-MB-468 cells as two genetically different models of TNBC. We employed various assays including Alamar Blue to measure the effect of SANG on cell viability and proliferation rate, flow cytometry analysis to study the potential of the compound to induce apoptosis and cell cycle arrest, quantitative qRT PCR apoptosis array to measure the expression of different genes mediating apoptosis, and the western system was used to analyze the impact of the compound on AKT protein expression. Results: SANG lowered cell viability and disrupted cell cycle progression in both cell lines. Furthermore, S-phase cell cycle arrest-mediated apoptosis was found to be the primary contributor to cell growth inhibition in MDA-MB-231 cells. SANG-treated TNBC cells showed significantly up-regulated mRNA expression of 18 genes associated with apoptosis, including eight TNF receptor superfamily (TNFRSF), three members of the BCL2 family, and two members of the caspase (CASP) family in MDA-MB-468 cells. In MDA-MB-231 cells, two members of the TNF superfamily and four members of the BCL2 family were affected. The western study data showed the inhibition of AKT protein expression in both cell lines concurrent with up-regulated BCL2L11 gene. Our results point to the AKT/PI3K signaling pathway as one of the key mechanisms behind SANG-induced cell cycle arrest and death. Conclusion: SANG shows anticancer properties and apoptosis-related gene expression changes in the two TNBC cell lines and suggests AKT/PI3K pathway implication in apoptosis induction and cell cycle arrest. Thus, we propose SANG's potential as a solitary or supplementary treatment agent against TNBC. In the United States, breast cancer (BC) is the most common malignancy and the second leading cause of death among women aged 20-59 years (1). Gene expression is controlled by molecular signal transduction, and alterations in transcriptional settings distinguish cancer cells (2). BC is a heterogeneous cancer type categorized based on its molecular features. Triple-negative breast cancer (TNBC) affects approximately 15% of patients with BC (2). However, the incidence of this subtype is two to three folds higher in African American (AA) women than in other ethnic groups (3, 4). TNBC is the most aggressive BC and has a poor outcome compared to different BC subtypes (3, 5). Based on immunohistochemical characteristics, the expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) are missing in TNBC cells (3, 6). Currently, chemotherapy is the principal treatment for patients with TNBC. However, disease recurrence can manifest within the first two years 323","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081022,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081022/thumbnails/1.jpg","file_name":"323.full.pdf","download_url":"https://www.academia.edu/attachments/119081022/download_file","bulk_download_file_name":"Involvement_of_AKT_PI3K_Pathway_in_Sangu.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081022/323.full-libre.pdf?1729611369=\u0026response-content-disposition=attachment%3B+filename%3DInvolvement_of_AKT_PI3K_Pathway_in_Sangu.pdf\u0026Expires=1742120023\u0026Signature=UoFUNoYPwnqxTHHDNhUxSxYe1FPKiZdMqMdWYEFyiH6P4bo8Ok-we9khg~AaZBy18QZyWNe0kkut9z4XWno0k3vN3hXukNImw1-QfXeIE2li5MdjdU6dHMU-ws2OdPzqyANoLBOTaDYh3b1FnS-kJpx1SnLSXsxqAwF0~l9nuOHMvDYTkKJ0YSrB9wVfRveMYfKKv7S41LbJ0X8C8hXAQwMbMf9lwExQqZhxq6bsBTIH~UGhMqOX4rFq2Aj1q4~RuINjLV7NHcksTYmFJokpTC9TgJA8p90Gm0YHIQEkgjQlzv36GnecY4FpsqTcYa7~BdY0pJ9LrxSqh0dKNx3e0Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":1290,"name":"Immunology","url":"https://www.academia.edu/Documents/in/Immunology"},{"id":9113,"name":"Cell Cycle","url":"https://www.academia.edu/Documents/in/Cell_Cycle"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"},{"id":1335152,"name":"Viability assay","url":"https://www.academia.edu/Documents/in/Viability_assay"}],"urls":[{"id":45280627,"url":"https://syndication.highwire.org/content/doi/10.21873/cgp.20385"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950490"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950490/Disparities_in_Infant_Nutrition_WIC_Participation_and_Rates_of_Breastfeeding_in_Florida"><img alt="Research paper thumbnail of Disparities in Infant Nutrition: WIC Participation and Rates of Breastfeeding in Florida" class="work-thumbnail" src="https://attachments.academia-assets.com/119080991/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950490/Disparities_in_Infant_Nutrition_WIC_Participation_and_Rates_of_Breastfeeding_in_Florida">Disparities in Infant Nutrition: WIC Participation and Rates of Breastfeeding in Florida</a></div><div class="wp-workCard_item"><span>International Journal of Environmental Research and Public Health</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Being cognizant of the pronounced health advantages of breastfeeding for both the nursing mother ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Being cognizant of the pronounced health advantages of breastfeeding for both the nursing mother and her infant, the breastfeeding dyad, we examined breastfeeding rates among Floridian women who gave birth from 2012 to 2014 (N = 639,052). We investigated the associations between breastfeeding initiation and WIC-based breastfeeding support (the Special Supplemental Nutrition Program for Women, Infants, and Children), education level, and race and ethnicity. We compared the percentage of breastfeeding mothers between those in the WIC program to those who were not, and we compared breastfeeding rates across racial and ethnic groups. Consistent with previous reports, black newborns in this study were breastfed at lower rates than other racial groups, and WIC program participants were less likely to breastfeed than non-WIC program participants. However, by breaking down the data by education level and race, and ethnicity, we see a significantly increased rate of breastfeeding due to WIC ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3a7c71c36da326db6a36429d3e2f4bcd" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119080991,"asset_id":124950490,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119080991/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950490"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950490"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950490; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950490]").text(description); $(".js-view-count[data-work-id=124950490]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950490; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950490']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "3a7c71c36da326db6a36429d3e2f4bcd" } } $('.js-work-strip[data-work-id=124950490]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950490,"title":"Disparities in Infant Nutrition: WIC Participation and Rates of Breastfeeding in Florida","translated_title":"","metadata":{"abstract":"Being cognizant of the pronounced health advantages of breastfeeding for both the nursing mother and her infant, the breastfeeding dyad, we examined breastfeeding rates among Floridian women who gave birth from 2012 to 2014 (N = 639,052). 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950489"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950489/Attenuative_Effect_of_Diallyl_Trisulfide_on_Caspase_Activity_in_TNF_%CE%B1_induced_Triple_Negative_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Attenuative Effect of Diallyl Trisulfide on Caspase Activity in TNF-α-induced Triple Negative Breast Cancer Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081020/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950489/Attenuative_Effect_of_Diallyl_Trisulfide_on_Caspase_Activity_in_TNF_%CE%B1_induced_Triple_Negative_Breast_Cancer_Cells">Attenuative Effect of Diallyl Trisulfide on Caspase Activity in TNF-α-induced Triple Negative Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>Anticancer Research</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit carcinogenesis in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit carcinogenesis in cancer cells. We have previously shown DATS's ability to decrease the percentage of viable cells, inhibit cell migration and modulate genes involved in the nuclear factor kappa-light-chainenhancer of activated B cells (NF-ĸB) and mitogen-activated protein kinase (MAPK) signaling. Materials and Methods: This study aimed to compare the efficacy of DATS in tumor necrosis factor alpha (TNF-α) induced MDA-MB-231 and MDA-MB-468 cells and investigate its role in cell-death signaling via cell cycle, flow cytometry, and caspase assay. Results: DATS exhibit a time-dependent accumulation of G 2 /M phase cells in both cell lines, with higher effects in the MDA-MB-468 for all time points. DATS's ability to decrease the percentage of viable cells in both MDA-MB-231 and MDA-MB-468 cells was shown by a significant but slight increase of early and late apoptosis in the presence of DATS compared to control. Moreover, MDA-MB-468 cells showed more sensitivity to the DATS effect, evidenced by the higher percentage of apoptosis than MDA-MB-231 cells. The caspase studies showed a significant increase in caspase 3 and 8 activity in the presence of DATS, compared to control, in both cell lines. DATS showed no significant increase in caspase 9 activity in both cell lines compared to the control. Conclusion: DATS-induced apoptosis in human breast cancer cells is mediated, at least in part, by cell cycle arrest and caspase activity. These findings provide information for future studies into the role of DATS in TNBC therapy and prevention.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="988ce306719a9cedfcc984b33df7c396" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081020,"asset_id":124950489,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081020/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950489"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950489"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950489; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950489]").text(description); $(".js-view-count[data-work-id=124950489]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950489; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950489']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "988ce306719a9cedfcc984b33df7c396" } } $('.js-work-strip[data-work-id=124950489]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950489,"title":"Attenuative Effect of Diallyl Trisulfide on Caspase Activity in TNF-α-induced Triple Negative Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Anticancer Research USA Inc.","ai_title_tag":"Diallyl Trisulfide Induces Apoptosis in TNF-α TNBC Cells","grobid_abstract":"Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit carcinogenesis in cancer cells. We have previously shown DATS's ability to decrease the percentage of viable cells, inhibit cell migration and modulate genes involved in the nuclear factor kappa-light-chainenhancer of activated B cells (NF-ĸB) and mitogen-activated protein kinase (MAPK) signaling. Materials and Methods: This study aimed to compare the efficacy of DATS in tumor necrosis factor alpha (TNF-α) induced MDA-MB-231 and MDA-MB-468 cells and investigate its role in cell-death signaling via cell cycle, flow cytometry, and caspase assay. Results: DATS exhibit a time-dependent accumulation of G 2 /M phase cells in both cell lines, with higher effects in the MDA-MB-468 for all time points. DATS's ability to decrease the percentage of viable cells in both MDA-MB-231 and MDA-MB-468 cells was shown by a significant but slight increase of early and late apoptosis in the presence of DATS compared to control. Moreover, MDA-MB-468 cells showed more sensitivity to the DATS effect, evidenced by the higher percentage of apoptosis than MDA-MB-231 cells. The caspase studies showed a significant increase in caspase 3 and 8 activity in the presence of DATS, compared to control, in both cell lines. DATS showed no significant increase in caspase 9 activity in both cell lines compared to the control. Conclusion: DATS-induced apoptosis in human breast cancer cells is mediated, at least in part, by cell cycle arrest and caspase activity. These findings provide information for future studies into the role of DATS in TNBC therapy and prevention.","publication_name":"Anticancer Research","grobid_abstract_attachment_id":119081020},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950489/Attenuative_Effect_of_Diallyl_Trisulfide_on_Caspase_Activity_in_TNF_%CE%B1_induced_Triple_Negative_Breast_Cancer_Cells","translated_internal_url":"","created_at":"2024-10-22T08:29:19.669-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081020,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081020/thumbnails/1.jpg","file_name":"2393.full.pdf","download_url":"https://www.academia.edu/attachments/119081020/download_file","bulk_download_file_name":"Attenuative_Effect_of_Diallyl_Trisulfide.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081020/2393.full-libre.pdf?1729611344=\u0026response-content-disposition=attachment%3B+filename%3DAttenuative_Effect_of_Diallyl_Trisulfide.pdf\u0026Expires=1742120023\u0026Signature=L2KAuCxb8ko7XWmyWxqHph7dIktaWkbl714ntLnrOAiLmDWDzcbxOeXHrQDJZA8Qwh3ocDiGJmTWGHBcRLZgL9nVBCXHAnbTqVJlcdSaVrNZf274RrWUchxKdQlU6MjyW0fiVb~sOC32LYkHyk9ns4H4tGPfb-2GqUSYOymva0gYc8F1srTopmwWXShl52KU~BFGf~RUT8BMChac1s925VuG8cKTR9l4JjGC95DbeRoVXjP2Q9jIoZUqAmGLoUMh0YB3MCtctASNPff1RKH51H3cC9FG5WPm3~EwgD10ENZHXCsfGl6nfAl~tmt3CqjXQH9frN5sriqQGhJbTn6WyA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Attenuative_Effect_of_Diallyl_Trisulfide_on_Caspase_Activity_in_TNF_α_induced_Triple_Negative_Breast_Cancer_Cells","translated_slug":"","page_count":13,"language":"en","content_type":"Work","summary":"Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit carcinogenesis in cancer cells. We have previously shown DATS's ability to decrease the percentage of viable cells, inhibit cell migration and modulate genes involved in the nuclear factor kappa-light-chainenhancer of activated B cells (NF-ĸB) and mitogen-activated protein kinase (MAPK) signaling. Materials and Methods: This study aimed to compare the efficacy of DATS in tumor necrosis factor alpha (TNF-α) induced MDA-MB-231 and MDA-MB-468 cells and investigate its role in cell-death signaling via cell cycle, flow cytometry, and caspase assay. Results: DATS exhibit a time-dependent accumulation of G 2 /M phase cells in both cell lines, with higher effects in the MDA-MB-468 for all time points. DATS's ability to decrease the percentage of viable cells in both MDA-MB-231 and MDA-MB-468 cells was shown by a significant but slight increase of early and late apoptosis in the presence of DATS compared to control. Moreover, MDA-MB-468 cells showed more sensitivity to the DATS effect, evidenced by the higher percentage of apoptosis than MDA-MB-231 cells. The caspase studies showed a significant increase in caspase 3 and 8 activity in the presence of DATS, compared to control, in both cell lines. DATS showed no significant increase in caspase 9 activity in both cell lines compared to the control. Conclusion: DATS-induced apoptosis in human breast cancer cells is mediated, at least in part, by cell cycle arrest and caspase activity. These findings provide information for future studies into the role of DATS in TNBC therapy and prevention.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081020,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081020/thumbnails/1.jpg","file_name":"2393.full.pdf","download_url":"https://www.academia.edu/attachments/119081020/download_file","bulk_download_file_name":"Attenuative_Effect_of_Diallyl_Trisulfide.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081020/2393.full-libre.pdf?1729611344=\u0026response-content-disposition=attachment%3B+filename%3DAttenuative_Effect_of_Diallyl_Trisulfide.pdf\u0026Expires=1742120023\u0026Signature=L2KAuCxb8ko7XWmyWxqHph7dIktaWkbl714ntLnrOAiLmDWDzcbxOeXHrQDJZA8Qwh3ocDiGJmTWGHBcRLZgL9nVBCXHAnbTqVJlcdSaVrNZf274RrWUchxKdQlU6MjyW0fiVb~sOC32LYkHyk9ns4H4tGPfb-2GqUSYOymva0gYc8F1srTopmwWXShl52KU~BFGf~RUT8BMChac1s925VuG8cKTR9l4JjGC95DbeRoVXjP2Q9jIoZUqAmGLoUMh0YB3MCtctASNPff1RKH51H3cC9FG5WPm3~EwgD10ENZHXCsfGl6nfAl~tmt3CqjXQH9frN5sriqQGhJbTn6WyA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":263843,"name":"Anticancer","url":"https://www.academia.edu/Documents/in/Anticancer"}],"urls":[{"id":45280625,"url":"https://syndication.highwire.org/content/doi/10.21873/anticanres.16407"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950488"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950488/Herbal_microbiomes_are_plant_specific_and_rich_in_immune_stimulating_pathogen_associated_molecular_pattern_molecules"><img alt="Research paper thumbnail of Herbal microbiomes are plant-specific and rich in immune-stimulating pathogen-associated molecular pattern molecules" class="work-thumbnail" src="https://attachments.academia-assets.com/119081021/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950488/Herbal_microbiomes_are_plant_specific_and_rich_in_immune_stimulating_pathogen_associated_molecular_pattern_molecules">Herbal microbiomes are plant-specific and rich in immune-stimulating pathogen-associated molecular pattern molecules</a></div><div class="wp-workCard_item"><span>ASPET 2023 Annual Meeting Abstract - Drug Discovery and Development</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ID 14491 Poster Board 296 For thousands of years, humans have been orally consuming herbal botani...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ID 14491 Poster Board 296 For thousands of years, humans have been orally consuming herbal botanical medicines, ascribing the beneficial effects to the plant itself. Oddly, we have not yet realized the impact of ingesting dead/live microorganisms in these plants. The residual dead remains of the herbal microbiome can and do leave a trail of thermal and pH-stable immune-stimulating antigenic epitopes with the capacity to act in the human gut. The current study employs a high throughput screening to elucidate the immune-stimulating properties of over-the-counter (OTC) / point-of-sale (POS) herbs. The findings illustrate the existence of an immune active herbal bioactive microbiome, which is plant specific but independent of the plant itself. In this study, an initial high throughput screening of 2535 phytochemicals and OTC/POS'S botanicals was carried out to elucidate pro-inflammatory effects in RAW 264.7 macrophages, with many as potent as positive controls: lipopolysaccharide (LPS) (E.coli 0111:B4). Microbial pathogen-associated molecular pattern molecules (PAMPS) in bio-active herbs were removed from the plants by spin column application, extracts were retested for a bioactive response, and the pH stability of LPS analyzed using a stomach simulation model. Lastly, we reverse cultured the "residual remains" in 7 OTC/POS herbs which were isolated, colonized, and sequenced using Illumina targeting the V4 region of the 16S rRNA gene and the V1-V3 region of the 18S rRNA gene. The obtained results show that Out of 2535 compounds screened, not a single phytochemical or drug (>500 tested) could mimic LPS, which was only observed for 65 "specific" herbal medicine plants, having high concentrations of PAMPS, dominating in roots and oceanic marine sea kelps /algae's [e.g.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="eb9dd3a2655b3df5aa8ad0279baca5b7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081021,"asset_id":124950488,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081021/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950488"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950488"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950488; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950488]").text(description); $(".js-view-count[data-work-id=124950488]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950488; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950488']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "eb9dd3a2655b3df5aa8ad0279baca5b7" } } $('.js-work-strip[data-work-id=124950488]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950488,"title":"Herbal microbiomes are plant-specific and rich in immune-stimulating pathogen-associated molecular pattern molecules","translated_title":"","metadata":{"publisher":"American Society for Pharmacology and Experimental Therapeutics","grobid_abstract":"ID 14491 Poster Board 296 For thousands of years, humans have been orally consuming herbal botanical medicines, ascribing the beneficial effects to the plant itself. Oddly, we have not yet realized the impact of ingesting dead/live microorganisms in these plants. The residual dead remains of the herbal microbiome can and do leave a trail of thermal and pH-stable immune-stimulating antigenic epitopes with the capacity to act in the human gut. The current study employs a high throughput screening to elucidate the immune-stimulating properties of over-the-counter (OTC) / point-of-sale (POS) herbs. The findings illustrate the existence of an immune active herbal bioactive microbiome, which is plant specific but independent of the plant itself. In this study, an initial high throughput screening of 2535 phytochemicals and OTC/POS'S botanicals was carried out to elucidate pro-inflammatory effects in RAW 264.7 macrophages, with many as potent as positive controls: lipopolysaccharide (LPS) (E.coli 0111:B4). Microbial pathogen-associated molecular pattern molecules (PAMPS) in bio-active herbs were removed from the plants by spin column application, extracts were retested for a bioactive response, and the pH stability of LPS analyzed using a stomach simulation model. Lastly, we reverse cultured the \"residual remains\" in 7 OTC/POS herbs which were isolated, colonized, and sequenced using Illumina targeting the V4 region of the 16S rRNA gene and the V1-V3 region of the 18S rRNA gene. The obtained results show that Out of 2535 compounds screened, not a single phytochemical or drug (\u003e500 tested) could mimic LPS, which was only observed for 65 \"specific\" herbal medicine plants, having high concentrations of PAMPS, dominating in roots and oceanic marine sea kelps /algae's [e.g.","publication_name":"ASPET 2023 Annual Meeting Abstract - Drug Discovery and Development","grobid_abstract_attachment_id":119081021},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950488/Herbal_microbiomes_are_plant_specific_and_rich_in_immune_stimulating_pathogen_associated_molecular_pattern_molecules","translated_internal_url":"","created_at":"2024-10-22T08:29:19.307-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081021,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081021/thumbnails/1.jpg","file_name":"296.full.pdf","download_url":"https://www.academia.edu/attachments/119081021/download_file","bulk_download_file_name":"Herbal_microbiomes_are_plant_specific_an.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081021/296.full-libre.pdf?1729611312=\u0026response-content-disposition=attachment%3B+filename%3DHerbal_microbiomes_are_plant_specific_an.pdf\u0026Expires=1742120023\u0026Signature=AuQmv6f4H7CXy4K4WVSgjV1dlme1i0FfPulsU4QnyrJOAbWmYD~vg3zlslikOLDXehyg7Z8eatYu59pIfpnnBmk2ybvHsG1JAyBFxfg2OPjfa8P8U0Cd9LU8RIVWSa7b7S4UuPEI1tExTiJdYJrkiiw6UIbP2wOhmf4Ch0WtcmujKRI-L7kQ8qYuyPiCxPOWdoC3OXiwyg9-pKjvUzQ8TacsifA70iyYfaV6u0JnUvQFGa016PBx5PRLBJbRlOTGdQAVDJiUN8cwIVSTguyILytcXlOU2nJ7lVrNHz~gvNuVOcdOz53lsO6M59td79La730l3Txv08mpXjctQTZKMA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Herbal_microbiomes_are_plant_specific_and_rich_in_immune_stimulating_pathogen_associated_molecular_pattern_molecules","translated_slug":"","page_count":1,"language":"en","content_type":"Work","summary":"ID 14491 Poster Board 296 For thousands of years, humans have been orally consuming herbal botanical medicines, ascribing the beneficial effects to the plant itself. Oddly, we have not yet realized the impact of ingesting dead/live microorganisms in these plants. The residual dead remains of the herbal microbiome can and do leave a trail of thermal and pH-stable immune-stimulating antigenic epitopes with the capacity to act in the human gut. The current study employs a high throughput screening to elucidate the immune-stimulating properties of over-the-counter (OTC) / point-of-sale (POS) herbs. The findings illustrate the existence of an immune active herbal bioactive microbiome, which is plant specific but independent of the plant itself. In this study, an initial high throughput screening of 2535 phytochemicals and OTC/POS'S botanicals was carried out to elucidate pro-inflammatory effects in RAW 264.7 macrophages, with many as potent as positive controls: lipopolysaccharide (LPS) (E.coli 0111:B4). Microbial pathogen-associated molecular pattern molecules (PAMPS) in bio-active herbs were removed from the plants by spin column application, extracts were retested for a bioactive response, and the pH stability of LPS analyzed using a stomach simulation model. Lastly, we reverse cultured the \"residual remains\" in 7 OTC/POS herbs which were isolated, colonized, and sequenced using Illumina targeting the V4 region of the 16S rRNA gene and the V1-V3 region of the 18S rRNA gene. The obtained results show that Out of 2535 compounds screened, not a single phytochemical or drug (\u003e500 tested) could mimic LPS, which was only observed for 65 \"specific\" herbal medicine plants, having high concentrations of PAMPS, dominating in roots and oceanic marine sea kelps /algae's [e.g.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081021,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081021/thumbnails/1.jpg","file_name":"296.full.pdf","download_url":"https://www.academia.edu/attachments/119081021/download_file","bulk_download_file_name":"Herbal_microbiomes_are_plant_specific_an.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081021/296.full-libre.pdf?1729611312=\u0026response-content-disposition=attachment%3B+filename%3DHerbal_microbiomes_are_plant_specific_an.pdf\u0026Expires=1742120023\u0026Signature=AuQmv6f4H7CXy4K4WVSgjV1dlme1i0FfPulsU4QnyrJOAbWmYD~vg3zlslikOLDXehyg7Z8eatYu59pIfpnnBmk2ybvHsG1JAyBFxfg2OPjfa8P8U0Cd9LU8RIVWSa7b7S4UuPEI1tExTiJdYJrkiiw6UIbP2wOhmf4Ch0WtcmujKRI-L7kQ8qYuyPiCxPOWdoC3OXiwyg9-pKjvUzQ8TacsifA70iyYfaV6u0JnUvQFGa016PBx5PRLBJbRlOTGdQAVDJiUN8cwIVSTguyILytcXlOU2nJ7lVrNHz~gvNuVOcdOz53lsO6M59td79La730l3Txv08mpXjctQTZKMA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":324154,"name":"Immune system","url":"https://www.academia.edu/Documents/in/Immune_system"},{"id":348435,"name":"Microbiome","url":"https://www.academia.edu/Documents/in/Microbiome"}],"urls":[{"id":45280624,"url":"https://syndication.highwire.org/content/doi/10.1124/jpet.122.144910"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950487"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950487/Prognostic_and_Therapeutic_Implications_of_Genes_Associated_with_Apoptosis_and_Protein_Protein_Interactions_in_Triple_Negative_Breast_Cancer"><img alt="Research paper thumbnail of Prognostic and Therapeutic Implications of Genes Associated with Apoptosis and Protein-Protein Interactions in Triple-Negative Breast Cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/119081019/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950487/Prognostic_and_Therapeutic_Implications_of_Genes_Associated_with_Apoptosis_and_Protein_Protein_Interactions_in_Triple_Negative_Breast_Cancer">Prognostic and Therapeutic Implications of Genes Associated with Apoptosis and Protein-Protein Interactions in Triple-Negative Breast Cancer</a></div><div class="wp-workCard_item"><span>ASPET 2023 Annual Meeting Abstract - Cancer Pharmacology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ID 54503 Poster Board 446 Triple-negative breast cancer (TNBC) has historically had fewer treatme...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ID 54503 Poster Board 446 Triple-negative breast cancer (TNBC) has historically had fewer treatment alternatives than other breast cancer types. Therefore, it is critical to explore and pinpoint potential biomarkers that could be utilized in treating TNBC. By doing this, we will significantly enhance a patient's prognosis and quality of life. Apoptosis-controlling genes could be manipulated to increase the death of cancer cells. It is essential to comprehend how the genes involved in the apoptotic pathway interact to identify potential therapeutic targets. Therefore, the current study is aimed to evaluate the gene expression, protein-protein interaction (PPI), and transcription factor interaction of 27 apoptosis-regulated genes in TNBC using integrated bioinformatics methods to assess the gene expression, protein-protein interaction (PPI) and transcription factor interaction. Our findings demonstrated that CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were substantially associated with the overall survival rate (OS) difference of TNBC patients. The results also show that breast tissue gene expressions of BNIP3, TNFRSF10B, MCL1, and CASP4 were downregulated compared to normal breast tissue in UALCAN. At the same time, BIK, AKT1, BAD, FADD, DIABLO, and CASP9 were downregulated in bc-GeneEx-Miner v4.5 mRNA expression (BCGM) databases. Based on the GO term enrichment analysis, the Cellular process (GO:0009987), which has about 21 apoptosis-regulated genes, is the top category in the biological process (BP), followed by biological regulation (GO:0065007). We identified 29 pathways, including p53, angiogenesis, and apoptosis signaling. We examined the PPIs between the genes that regulate apoptosis; CASP3 and CASP9 interact with FADD, MCL1, TNF, TNFRSRF10A, and TNFRSF10; additionally, CASP3 significantly forms PPIs with CASP9, DFFA, and TP53, while CASP9 with DIABLO. In the top 10 transcription factors, the androgen receptor (AR) interacts with five apoptosis-regulated genes (p<0.0001; q<0.01), followed by RARA (Retinoic Acid Receptor Alpha) (p<0.0001; q<0.01) and RNF2 (Ring Finger Protein) (p<0.0001; q<0.01). Overall, the gene expression profile, the PPIs, and the apoptosis-TF interaction findings suggested that the 27 apoptosis-regulated genes might be used as promising targets in treating and managing TNBC. Furthermore, from a total of 27 key genes, CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were significantly correlated with poor overall survival in TNBC (p-value < 0.05), which could play essential roles in the progression of TNBC and provide attractive therapeutic targets that may offer new candidate molecules for targeted therapy. It was concluded from this study that genetic alterations altering apoptosis could be possible biomarkers for the prognosis and facilitate the search for alternative treatment targets for TNBC.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="575df43c5467fd03d435f17615d9ac93" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081019,"asset_id":124950487,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081019/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950487"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950487"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950487; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950487]").text(description); $(".js-view-count[data-work-id=124950487]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950487; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950487']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "575df43c5467fd03d435f17615d9ac93" } } $('.js-work-strip[data-work-id=124950487]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950487,"title":"Prognostic and Therapeutic Implications of Genes Associated with Apoptosis and Protein-Protein Interactions in Triple-Negative Breast Cancer","translated_title":"","metadata":{"publisher":"American Society for Pharmacology and Experimental Therapeutics","grobid_abstract":"ID 54503 Poster Board 446 Triple-negative breast cancer (TNBC) has historically had fewer treatment alternatives than other breast cancer types. Therefore, it is critical to explore and pinpoint potential biomarkers that could be utilized in treating TNBC. By doing this, we will significantly enhance a patient's prognosis and quality of life. Apoptosis-controlling genes could be manipulated to increase the death of cancer cells. It is essential to comprehend how the genes involved in the apoptotic pathway interact to identify potential therapeutic targets. Therefore, the current study is aimed to evaluate the gene expression, protein-protein interaction (PPI), and transcription factor interaction of 27 apoptosis-regulated genes in TNBC using integrated bioinformatics methods to assess the gene expression, protein-protein interaction (PPI) and transcription factor interaction. Our findings demonstrated that CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were substantially associated with the overall survival rate (OS) difference of TNBC patients. The results also show that breast tissue gene expressions of BNIP3, TNFRSF10B, MCL1, and CASP4 were downregulated compared to normal breast tissue in UALCAN. At the same time, BIK, AKT1, BAD, FADD, DIABLO, and CASP9 were downregulated in bc-GeneEx-Miner v4.5 mRNA expression (BCGM) databases. Based on the GO term enrichment analysis, the Cellular process (GO:0009987), which has about 21 apoptosis-regulated genes, is the top category in the biological process (BP), followed by biological regulation (GO:0065007). We identified 29 pathways, including p53, angiogenesis, and apoptosis signaling. We examined the PPIs between the genes that regulate apoptosis; CASP3 and CASP9 interact with FADD, MCL1, TNF, TNFRSRF10A, and TNFRSF10; additionally, CASP3 significantly forms PPIs with CASP9, DFFA, and TP53, while CASP9 with DIABLO. In the top 10 transcription factors, the androgen receptor (AR) interacts with five apoptosis-regulated genes (p\u003c0.0001; q\u003c0.01), followed by RARA (Retinoic Acid Receptor Alpha) (p\u003c0.0001; q\u003c0.01) and RNF2 (Ring Finger Protein) (p\u003c0.0001; q\u003c0.01). Overall, the gene expression profile, the PPIs, and the apoptosis-TF interaction findings suggested that the 27 apoptosis-regulated genes might be used as promising targets in treating and managing TNBC. Furthermore, from a total of 27 key genes, CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were significantly correlated with poor overall survival in TNBC (p-value \u003c 0.05), which could play essential roles in the progression of TNBC and provide attractive therapeutic targets that may offer new candidate molecules for targeted therapy. 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Therefore, it is critical to explore and pinpoint potential biomarkers that could be utilized in treating TNBC. By doing this, we will significantly enhance a patient's prognosis and quality of life. Apoptosis-controlling genes could be manipulated to increase the death of cancer cells. It is essential to comprehend how the genes involved in the apoptotic pathway interact to identify potential therapeutic targets. Therefore, the current study is aimed to evaluate the gene expression, protein-protein interaction (PPI), and transcription factor interaction of 27 apoptosis-regulated genes in TNBC using integrated bioinformatics methods to assess the gene expression, protein-protein interaction (PPI) and transcription factor interaction. Our findings demonstrated that CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were substantially associated with the overall survival rate (OS) difference of TNBC patients. The results also show that breast tissue gene expressions of BNIP3, TNFRSF10B, MCL1, and CASP4 were downregulated compared to normal breast tissue in UALCAN. At the same time, BIK, AKT1, BAD, FADD, DIABLO, and CASP9 were downregulated in bc-GeneEx-Miner v4.5 mRNA expression (BCGM) databases. Based on the GO term enrichment analysis, the Cellular process (GO:0009987), which has about 21 apoptosis-regulated genes, is the top category in the biological process (BP), followed by biological regulation (GO:0065007). We identified 29 pathways, including p53, angiogenesis, and apoptosis signaling. We examined the PPIs between the genes that regulate apoptosis; CASP3 and CASP9 interact with FADD, MCL1, TNF, TNFRSRF10A, and TNFRSF10; additionally, CASP3 significantly forms PPIs with CASP9, DFFA, and TP53, while CASP9 with DIABLO. In the top 10 transcription factors, the androgen receptor (AR) interacts with five apoptosis-regulated genes (p\u003c0.0001; q\u003c0.01), followed by RARA (Retinoic Acid Receptor Alpha) (p\u003c0.0001; q\u003c0.01) and RNF2 (Ring Finger Protein) (p\u003c0.0001; q\u003c0.01). Overall, the gene expression profile, the PPIs, and the apoptosis-TF interaction findings suggested that the 27 apoptosis-regulated genes might be used as promising targets in treating and managing TNBC. Furthermore, from a total of 27 key genes, CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were significantly correlated with poor overall survival in TNBC (p-value \u003c 0.05), which could play essential roles in the progression of TNBC and provide attractive therapeutic targets that may offer new candidate molecules for targeted therapy. It was concluded from this study that genetic alterations altering apoptosis could be possible biomarkers for the prognosis and facilitate the search for alternative treatment targets for TNBC.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081019,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081019/thumbnails/1.jpg","file_name":"446.full.pdf","download_url":"https://www.academia.edu/attachments/119081019/download_file","bulk_download_file_name":"Prognostic_and_Therapeutic_Implications.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081019/446.full-libre.pdf?1729611315=\u0026response-content-disposition=attachment%3B+filename%3DPrognostic_and_Therapeutic_Implications.pdf\u0026Expires=1742120023\u0026Signature=Fg2o4XElxETn3I~etDfPU67iwKaL1anjjl9uJEJ4LR8g-6KesvHNAlvYm7InnHfUxP-dQpS1yjvLPPldLTL~ajFhzVhD06CLga2VffzRzwwtN0omNAfeMGICcwF0UdCZn-hM1dUakvfb6ZPMHocNUBCTHG3ZmV3ulySp744SrnMcPKMeMHftKYm7SIkivRNa~wziSm~ML3E4SUr8UWhwyDHeBZ1ZhtCG1zwYx~gszLSJstUbNOKCWVPUe0-SuAa6w-TAaazv8SYlLrVvoPwKCniZn6FHxv~VAP6ci0oiZc3J-WYSg0XHEb1VSWO~YhuaxTr6NgpdCP1kQuUs6pPkwQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":6802,"name":"Breast Cancer","url":"https://www.academia.edu/Documents/in/Breast_Cancer"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":181936,"name":"Gene","url":"https://www.academia.edu/Documents/in/Gene"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"}],"urls":[{"id":45280623,"url":"https://syndication.highwire.org/content/doi/10.1124/jpet.122.545030"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950486"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950486/Transcriptome_Profiling_During_Muscadine_Berry_Development_Reveals_the_Dynamic_of_Polyphenols_Metabolism"><img alt="Research paper thumbnail of Transcriptome Profiling During Muscadine Berry Development Reveals the Dynamic of Polyphenols Metabolism" class="work-thumbnail" src="https://attachments.academia-assets.com/119081016/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950486/Transcriptome_Profiling_During_Muscadine_Berry_Development_Reveals_the_Dynamic_of_Polyphenols_Metabolism">Transcriptome Profiling During Muscadine Berry Development Reveals the Dynamic of Polyphenols Metabolism</a></div><div class="wp-workCard_item"><span>Frontiers in Plant Science</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape speci...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape species. To identify the molecular events associated with polyphenolic accumulation that influence antioxidant capacity, two contrasting muscadine genotypes (C5 and C6) with varied phenolic/flavonoid content and antioxidant activity were investigatedviaRNA-sequencing during berry development. The results showed that berry development is concomitant with transcriptome profile changes, which was more pronounced at the véraison (V) stage. Despite that the downregulation pattern of gene expression dominated the upregulation through berry development, the C5 genotype maintained higher expression levels. Comparative transcript profiling allowed the identification of 94 differentially expressed genes with potential relevance in regulating fruit secondary metabolism, including 18 transcription factors and 76 structural genes. The genes underlying the critical enzymes in the modification reactions of ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="6c1adeb698213f60edf3e33711043a45" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081016,"asset_id":124950486,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081016/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950486"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950486"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950486; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950486]").text(description); $(".js-view-count[data-work-id=124950486]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950486; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950486']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "6c1adeb698213f60edf3e33711043a45" } } $('.js-work-strip[data-work-id=124950486]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950486,"title":"Transcriptome Profiling During Muscadine Berry Development Reveals the Dynamic of Polyphenols Metabolism","translated_title":"","metadata":{"abstract":"Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape species. To identify the molecular events associated with polyphenolic accumulation that influence antioxidant capacity, two contrasting muscadine genotypes (C5 and C6) with varied phenolic/flavonoid content and antioxidant activity were investigatedviaRNA-sequencing during berry development. The results showed that berry development is concomitant with transcriptome profile changes, which was more pronounced at the véraison (V) stage. Despite that the downregulation pattern of gene expression dominated the upregulation through berry development, the C5 genotype maintained higher expression levels. Comparative transcript profiling allowed the identification of 94 differentially expressed genes with potential relevance in regulating fruit secondary metabolism, including 18 transcription factors and 76 structural genes. The genes underlying the critical enzymes in the modification reactions of ...","publisher":"Frontiers Media SA","publication_name":"Frontiers in Plant Science"},"translated_abstract":"Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape species. To identify the molecular events associated with polyphenolic accumulation that influence antioxidant capacity, two contrasting muscadine genotypes (C5 and C6) with varied phenolic/flavonoid content and antioxidant activity were investigatedviaRNA-sequencing during berry development. The results showed that berry development is concomitant with transcriptome profile changes, which was more pronounced at the véraison (V) stage. Despite that the downregulation pattern of gene expression dominated the upregulation through berry development, the C5 genotype maintained higher expression levels. Comparative transcript profiling allowed the identification of 94 differentially expressed genes with potential relevance in regulating fruit secondary metabolism, including 18 transcription factors and 76 structural genes. The genes underlying the critical enzymes in the modification reactions of ...","internal_url":"https://www.academia.edu/124950486/Transcriptome_Profiling_During_Muscadine_Berry_Development_Reveals_the_Dynamic_of_Polyphenols_Metabolism","translated_internal_url":"","created_at":"2024-10-22T08:29:18.750-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081016,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081016/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081016/download_file","bulk_download_file_name":"Transcriptome_Profiling_During_Muscadine.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081016/pdf-libre.pdf?1729611330=\u0026response-content-disposition=attachment%3B+filename%3DTranscriptome_Profiling_During_Muscadine.pdf\u0026Expires=1742120023\u0026Signature=PXAezDil4kGIZ2H-3zgmcWvrW2VJ-r-wIM3qPLcVFRGTfscu2VAQuOTv7Uvhq5RD2FAcrBAi-J0D6x8mTH1K1nFi4oExgaHdeAYg00nyT7gq~pM47-UJNHyONMnqgKSKiVyADlzs9jfCX6tek~TSQhrXUy~6KBuy15mbWGIC51sfkTAkMg3~kCNne9-xz0e~OZto0ALcyebstB-4U0jNlBIbtmMbylmnLWJThE0qS2uo7L6lTo87E06xSmoBB92-4QVzpR-tEpHaPTKET0ijBosZil2gv0kcyRd92Fk5MLao3YI8M-9RD1S5bvHHqc00qRK3e4b2HFYCRgFMvWaNsA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Transcriptome_Profiling_During_Muscadine_Berry_Development_Reveals_the_Dynamic_of_Polyphenols_Metabolism","translated_slug":"","page_count":17,"language":"en","content_type":"Work","summary":"Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape species. To identify the molecular events associated with polyphenolic accumulation that influence antioxidant capacity, two contrasting muscadine genotypes (C5 and C6) with varied phenolic/flavonoid content and antioxidant activity were investigatedviaRNA-sequencing during berry development. The results showed that berry development is concomitant with transcriptome profile changes, which was more pronounced at the véraison (V) stage. Despite that the downregulation pattern of gene expression dominated the upregulation through berry development, the C5 genotype maintained higher expression levels. Comparative transcript profiling allowed the identification of 94 differentially expressed genes with potential relevance in regulating fruit secondary metabolism, including 18 transcription factors and 76 structural genes. The genes underlying the critical enzymes in the modification reactions of ...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081016,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081016/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081016/download_file","bulk_download_file_name":"Transcriptome_Profiling_During_Muscadine.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081016/pdf-libre.pdf?1729611330=\u0026response-content-disposition=attachment%3B+filename%3DTranscriptome_Profiling_During_Muscadine.pdf\u0026Expires=1742120023\u0026Signature=PXAezDil4kGIZ2H-3zgmcWvrW2VJ-r-wIM3qPLcVFRGTfscu2VAQuOTv7Uvhq5RD2FAcrBAi-J0D6x8mTH1K1nFi4oExgaHdeAYg00nyT7gq~pM47-UJNHyONMnqgKSKiVyADlzs9jfCX6tek~TSQhrXUy~6KBuy15mbWGIC51sfkTAkMg3~kCNne9-xz0e~OZto0ALcyebstB-4U0jNlBIbtmMbylmnLWJThE0qS2uo7L6lTo87E06xSmoBB92-4QVzpR-tEpHaPTKET0ijBosZil2gv0kcyRd92Fk5MLao3YI8M-9RD1S5bvHHqc00qRK3e4b2HFYCRgFMvWaNsA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":43761,"name":"Transcriptome","url":"https://www.academia.edu/Documents/in/Transcriptome"},{"id":94697,"name":"Plant Secondary Metabolism","url":"https://www.academia.edu/Documents/in/Plant_Secondary_Metabolism"},{"id":732057,"name":"Flavonoid","url":"https://www.academia.edu/Documents/in/Flavonoid"},{"id":832148,"name":"Polyphenol","url":"https://www.academia.edu/Documents/in/Polyphenol"},{"id":980353,"name":"Berry","url":"https://www.academia.edu/Documents/in/Berry"},{"id":1810445,"name":"Gene expression profiling","url":"https://www.academia.edu/Documents/in/Gene_expression_profiling"}],"urls":[{"id":45280622,"url":"https://www.frontiersin.org/articles/10.3389/fpls.2021.818071/full"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950485"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950485/A_multi_locus_genome_wide_association_study_reveals_the_genetics_underlying_muscadine_antioxidant_in_berry_skin"><img alt="Research paper thumbnail of A multi-locus genome-wide association study reveals the genetics underlying muscadine antioxidant in berry skin" class="work-thumbnail" src="https://attachments.academia-assets.com/119081017/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950485/A_multi_locus_genome_wide_association_study_reveals_the_genetics_underlying_muscadine_antioxidant_in_berry_skin">A multi-locus genome-wide association study reveals the genetics underlying muscadine antioxidant in berry skin</a></div><div class="wp-workCard_item"><span>Frontiers in Plant Science</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phy...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phytochemical constituents with great potential antioxidant activity. Such nutritional and health merits are not only restricted to muscadine, but muscadine berries accumulate higher amounts of bioactive polyphenolics compared with other grape species. For the genetic study of the antioxidant trait in muscadine, a multi-locus genome-wide association study (GWAS) with 350 muscadine genotypes and 1,283 RNase H2 enzyme-dependent amplicon sequencing (rhAmpSeq) markers was performed. Phenotyping was conducted with several antioxidant-related traits, including total phenolic content (TPC), total flavonoid content (TFC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity, and FRAP antioxidant assay in muscadine berry skin. The correlation coefficient analysis revealed that the TPC, and DPPH/FRAP activities were significantly correlated. Through the GWAS analysis, 12 QTNs were id...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="35f8ee2e9ef448c0acd58cf64ba4d046" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081017,"asset_id":124950485,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081017/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950485"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950485"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950485; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950485]").text(description); $(".js-view-count[data-work-id=124950485]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950485; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950485']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "35f8ee2e9ef448c0acd58cf64ba4d046" } } $('.js-work-strip[data-work-id=124950485]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950485,"title":"A multi-locus genome-wide association study reveals the genetics underlying muscadine antioxidant in berry skin","translated_title":"","metadata":{"abstract":"Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phytochemical constituents with great potential antioxidant activity. Such nutritional and health merits are not only restricted to muscadine, but muscadine berries accumulate higher amounts of bioactive polyphenolics compared with other grape species. For the genetic study of the antioxidant trait in muscadine, a multi-locus genome-wide association study (GWAS) with 350 muscadine genotypes and 1,283 RNase H2 enzyme-dependent amplicon sequencing (rhAmpSeq) markers was performed. Phenotyping was conducted with several antioxidant-related traits, including total phenolic content (TPC), total flavonoid content (TFC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity, and FRAP antioxidant assay in muscadine berry skin. The correlation coefficient analysis revealed that the TPC, and DPPH/FRAP activities were significantly correlated. Through the GWAS analysis, 12 QTNs were id...","publisher":"Frontiers Media SA","publication_name":"Frontiers in Plant Science"},"translated_abstract":"Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phytochemical constituents with great potential antioxidant activity. Such nutritional and health merits are not only restricted to muscadine, but muscadine berries accumulate higher amounts of bioactive polyphenolics compared with other grape species. For the genetic study of the antioxidant trait in muscadine, a multi-locus genome-wide association study (GWAS) with 350 muscadine genotypes and 1,283 RNase H2 enzyme-dependent amplicon sequencing (rhAmpSeq) markers was performed. Phenotyping was conducted with several antioxidant-related traits, including total phenolic content (TPC), total flavonoid content (TFC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity, and FRAP antioxidant assay in muscadine berry skin. The correlation coefficient analysis revealed that the TPC, and DPPH/FRAP activities were significantly correlated. Through the GWAS analysis, 12 QTNs were id...","internal_url":"https://www.academia.edu/124950485/A_multi_locus_genome_wide_association_study_reveals_the_genetics_underlying_muscadine_antioxidant_in_berry_skin","translated_internal_url":"","created_at":"2024-10-22T08:29:18.483-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081017,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081017/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081017/download_file","bulk_download_file_name":"A_multi_locus_genome_wide_association_st.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081017/pdf-libre.pdf?1729611330=\u0026response-content-disposition=attachment%3B+filename%3DA_multi_locus_genome_wide_association_st.pdf\u0026Expires=1742120023\u0026Signature=IL-IOHijvakpYD0x8HQHqJI897oxKZzn5mqg0Am0ezoJgSGq29ydv1r~Ikajrnzliu~yduoxBTPq7fYKRmz3UoGrm8ZWV2lU1Y8mh79-dAegR6jb62ynIFTzsUvFzoPXLbT7izcx2n1Jo45gG2oqc-t2c~IfLKyr9GxkkZgTwkk0PE7QFew1e8sjWfTxc-sxTNIHL30y3tM6193JkrOQ2j5hi22A2SIZAN4gOM6rdxVDjNkJaQ3t7VkcFxw7UMke~xpd4aHymYpuc7oWCSuzJLfpv9lBRRYT0R3gNGSWUvXnc6SwzsRF0DsKV0OSz85JWkGtLbw4GQFik6DwA4v12w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"A_multi_locus_genome_wide_association_study_reveals_the_genetics_underlying_muscadine_antioxidant_in_berry_skin","translated_slug":"","page_count":12,"language":"en","content_type":"Work","summary":"Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phytochemical constituents with great potential antioxidant activity. Such nutritional and health merits are not only restricted to muscadine, but muscadine berries accumulate higher amounts of bioactive polyphenolics compared with other grape species. For the genetic study of the antioxidant trait in muscadine, a multi-locus genome-wide association study (GWAS) with 350 muscadine genotypes and 1,283 RNase H2 enzyme-dependent amplicon sequencing (rhAmpSeq) markers was performed. Phenotyping was conducted with several antioxidant-related traits, including total phenolic content (TPC), total flavonoid content (TFC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity, and FRAP antioxidant assay in muscadine berry skin. The correlation coefficient analysis revealed that the TPC, and DPPH/FRAP activities were significantly correlated. Through the GWAS analysis, 12 QTNs were id...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081017,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081017/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081017/download_file","bulk_download_file_name":"A_multi_locus_genome_wide_association_st.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081017/pdf-libre.pdf?1729611330=\u0026response-content-disposition=attachment%3B+filename%3DA_multi_locus_genome_wide_association_st.pdf\u0026Expires=1742120023\u0026Signature=IL-IOHijvakpYD0x8HQHqJI897oxKZzn5mqg0Am0ezoJgSGq29ydv1r~Ikajrnzliu~yduoxBTPq7fYKRmz3UoGrm8ZWV2lU1Y8mh79-dAegR6jb62ynIFTzsUvFzoPXLbT7izcx2n1Jo45gG2oqc-t2c~IfLKyr9GxkkZgTwkk0PE7QFew1e8sjWfTxc-sxTNIHL30y3tM6193JkrOQ2j5hi22A2SIZAN4gOM6rdxVDjNkJaQ3t7VkcFxw7UMke~xpd4aHymYpuc7oWCSuzJLfpv9lBRRYT0R3gNGSWUvXnc6SwzsRF0DsKV0OSz85JWkGtLbw4GQFik6DwA4v12w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":382472,"name":"DPPH","url":"https://www.academia.edu/Documents/in/DPPH"}],"urls":[{"id":45280621,"url":"https://www.frontiersin.org/articles/10.3389/fpls.2022.969301/full"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950484"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950484/Abstract_PO_116_Pentagalloyl_glucose_inhibits_GRO_%CE%B1_CXCL1_pro_inflammatory_cytokine_and_induces_expression_of_apoptosis_related_genes_in_racially_different_TNBC_cells"><img alt="Research paper thumbnail of Abstract PO-116: Pentagalloyl glucose inhibits GRO-α/CXCL1 pro-inflammatory cytokine and induces expression of apoptosis-related genes in racially different TNBC cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950484/Abstract_PO_116_Pentagalloyl_glucose_inhibits_GRO_%CE%B1_CXCL1_pro_inflammatory_cytokine_and_induces_expression_of_apoptosis_related_genes_in_racially_different_TNBC_cells">Abstract PO-116: Pentagalloyl glucose inhibits GRO-α/CXCL1 pro-inflammatory cytokine and induces expression of apoptosis-related genes in racially different TNBC cells</a></div><div class="wp-workCard_item"><span>Cancer Epidemiology, Biomarkers &amp; Prevention</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A distinctive tumor microenvironment associated with chronic inflammation, cancer development, an...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A distinctive tumor microenvironment associated with chronic inflammation, cancer development, and drug resistance in triple-negative breast cancer (TNBC) affect disproportionally Caucasian and African American women. PURPOSE: This investigation presents possible new biomarkers that could be modulated by the natural compound pentagalloyl glucose (PGG) in MM-231 (Caucasians) and MM-468 (African American) TNBC cells. METHODS: Cytokine arrays, ELISA, RT-PCR, flow cytometry, and Western analysis were performed. RESULTS: PGG reduced the expression of GRO-α/CXCL1 pro-inflammatory cytokine, which is associated with tumor recurrence and chemoresistance. PGG inhibited IκBKE and MAPK1 gene and protein expression indicating a possible signaling pathway for CXCL1 downregulation through NFκB and MAPK signaling. PGG also inhibited cell growth in both cell lines, which could be associated with a decrease in CXCL1 levels. Besides, PGG induced apoptosis, modulating numerous genes, including caspases...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950484"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950484"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950484; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950484]").text(description); $(".js-view-count[data-work-id=124950484]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950484; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950484']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950484]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950484,"title":"Abstract PO-116: Pentagalloyl glucose inhibits GRO-α/CXCL1 pro-inflammatory cytokine and induces expression of apoptosis-related genes in racially different TNBC cells","translated_title":"","metadata":{"abstract":"A distinctive tumor microenvironment associated with chronic inflammation, cancer development, and drug resistance in triple-negative breast cancer (TNBC) affect disproportionally Caucasian and African American women. PURPOSE: This investigation presents possible new biomarkers that could be modulated by the natural compound pentagalloyl glucose (PGG) in MM-231 (Caucasians) and MM-468 (African American) TNBC cells. METHODS: Cytokine arrays, ELISA, RT-PCR, flow cytometry, and Western analysis were performed. RESULTS: PGG reduced the expression of GRO-α/CXCL1 pro-inflammatory cytokine, which is associated with tumor recurrence and chemoresistance. PGG inhibited IκBKE and MAPK1 gene and protein expression indicating a possible signaling pathway for CXCL1 downregulation through NFκB and MAPK signaling. PGG also inhibited cell growth in both cell lines, which could be associated with a decrease in CXCL1 levels. Besides, PGG induced apoptosis, modulating numerous genes, including caspases...","publisher":"American Association for Cancer Research (AACR)","publication_name":"Cancer Epidemiology, Biomarkers \u0026amp; Prevention"},"translated_abstract":"A distinctive tumor microenvironment associated with chronic inflammation, cancer development, and drug resistance in triple-negative breast cancer (TNBC) affect disproportionally Caucasian and African American women. PURPOSE: This investigation presents possible new biomarkers that could be modulated by the natural compound pentagalloyl glucose (PGG) in MM-231 (Caucasians) and MM-468 (African American) TNBC cells. METHODS: Cytokine arrays, ELISA, RT-PCR, flow cytometry, and Western analysis were performed. RESULTS: PGG reduced the expression of GRO-α/CXCL1 pro-inflammatory cytokine, which is associated with tumor recurrence and chemoresistance. PGG inhibited IκBKE and MAPK1 gene and protein expression indicating a possible signaling pathway for CXCL1 downregulation through NFκB and MAPK signaling. PGG also inhibited cell growth in both cell lines, which could be associated with a decrease in CXCL1 levels. Besides, PGG induced apoptosis, modulating numerous genes, including caspases...","internal_url":"https://www.academia.edu/124950484/Abstract_PO_116_Pentagalloyl_glucose_inhibits_GRO_%CE%B1_CXCL1_pro_inflammatory_cytokine_and_induces_expression_of_apoptosis_related_genes_in_racially_different_TNBC_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:18.240-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Abstract_PO_116_Pentagalloyl_glucose_inhibits_GRO_α_CXCL1_pro_inflammatory_cytokine_and_induces_expression_of_apoptosis_related_genes_in_racially_different_TNBC_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"A distinctive tumor microenvironment associated with chronic inflammation, cancer development, and drug resistance in triple-negative breast cancer (TNBC) affect disproportionally Caucasian and African American women. PURPOSE: This investigation presents possible new biomarkers that could be modulated by the natural compound pentagalloyl glucose (PGG) in MM-231 (Caucasians) and MM-468 (African American) TNBC cells. METHODS: Cytokine arrays, ELISA, RT-PCR, flow cytometry, and Western analysis were performed. RESULTS: PGG reduced the expression of GRO-α/CXCL1 pro-inflammatory cytokine, which is associated with tumor recurrence and chemoresistance. PGG inhibited IκBKE and MAPK1 gene and protein expression indicating a possible signaling pathway for CXCL1 downregulation through NFκB and MAPK signaling. PGG also inhibited cell growth in both cell lines, which could be associated with a decrease in CXCL1 levels. Besides, PGG induced apoptosis, modulating numerous genes, including caspases...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":295233,"name":"Cytokine","url":"https://www.academia.edu/Documents/in/Cytokine"},{"id":474029,"name":"Tumor necrosis factor-alpha","url":"https://www.academia.edu/Documents/in/Tumor_necrosis_factor-alpha"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":45280620,"url":"https://aacrjournals.org/cebp/article/29/12_Supplement/PO-116/181620/Abstract-PO-116-Pentagalloyl-glucose-inhibits-GRO"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950483"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950483/Abstract_PO_132_Rosmarinic_acid_induced_apoptosis_and_cell_cycle_arrest_in_triple_negative_breast_cancer_cells"><img alt="Research paper thumbnail of Abstract PO-132: Rosmarinic acid-induced apoptosis and cell cycle arrest in triple-negative breast cancer cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950483/Abstract_PO_132_Rosmarinic_acid_induced_apoptosis_and_cell_cycle_arrest_in_triple_negative_breast_cancer_cells">Abstract PO-132: Rosmarinic acid-induced apoptosis and cell cycle arrest in triple-negative breast cancer cells</a></div><div class="wp-workCard_item"><span>Cancer Epidemiology, Biomarkers &amp; Prevention</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, includin...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, including anti-inflammatory, immunomodulatory, anti-mutagenic, antioxidant, and anticancer activities. This study evaluated the effects of RA in two racially different triple-negative breast cancer (TNBC) cell lines. One cell line was derived from Caucasian origin (MDA-MB-231), and another one was derived from an African American origin (MDA-MB-468). The apoptotic effect of RA was performed using An Annexin V-FITC Apoptosis Detection Kit, while the Propidium Iodide Flow Cytometry Kit was used to detect the cell cycle distribution. Gene expression profiling was established using Human Apoptosis PCR array. The results obtained show that RA significantly caused cytotoxic and antiproliferative effects in both cell lines in a dose- and time-dependent manner. It was noted that RA induced cell cycle arrest-related apoptosis and altered the expression of many apoptosis-involved genes differently. In MDA...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950483"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950483"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950483; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950483]").text(description); $(".js-view-count[data-work-id=124950483]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950483; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950483']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950483]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950483,"title":"Abstract PO-132: Rosmarinic acid-induced apoptosis and cell cycle arrest in triple-negative breast cancer cells","translated_title":"","metadata":{"abstract":"Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, including anti-inflammatory, immunomodulatory, anti-mutagenic, antioxidant, and anticancer activities. This study evaluated the effects of RA in two racially different triple-negative breast cancer (TNBC) cell lines. One cell line was derived from Caucasian origin (MDA-MB-231), and another one was derived from an African American origin (MDA-MB-468). The apoptotic effect of RA was performed using An Annexin V-FITC Apoptosis Detection Kit, while the Propidium Iodide Flow Cytometry Kit was used to detect the cell cycle distribution. Gene expression profiling was established using Human Apoptosis PCR array. The results obtained show that RA significantly caused cytotoxic and antiproliferative effects in both cell lines in a dose- and time-dependent manner. It was noted that RA induced cell cycle arrest-related apoptosis and altered the expression of many apoptosis-involved genes differently. In MDA...","publisher":"American Association for Cancer Research (AACR)","publication_name":"Cancer Epidemiology, Biomarkers \u0026amp; Prevention"},"translated_abstract":"Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, including anti-inflammatory, immunomodulatory, anti-mutagenic, antioxidant, and anticancer activities. This study evaluated the effects of RA in two racially different triple-negative breast cancer (TNBC) cell lines. One cell line was derived from Caucasian origin (MDA-MB-231), and another one was derived from an African American origin (MDA-MB-468). The apoptotic effect of RA was performed using An Annexin V-FITC Apoptosis Detection Kit, while the Propidium Iodide Flow Cytometry Kit was used to detect the cell cycle distribution. Gene expression profiling was established using Human Apoptosis PCR array. The results obtained show that RA significantly caused cytotoxic and antiproliferative effects in both cell lines in a dose- and time-dependent manner. It was noted that RA induced cell cycle arrest-related apoptosis and altered the expression of many apoptosis-involved genes differently. In MDA...","internal_url":"https://www.academia.edu/124950483/Abstract_PO_132_Rosmarinic_acid_induced_apoptosis_and_cell_cycle_arrest_in_triple_negative_breast_cancer_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:17.965-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Abstract_PO_132_Rosmarinic_acid_induced_apoptosis_and_cell_cycle_arrest_in_triple_negative_breast_cancer_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, including anti-inflammatory, immunomodulatory, anti-mutagenic, antioxidant, and anticancer activities. This study evaluated the effects of RA in two racially different triple-negative breast cancer (TNBC) cell lines. One cell line was derived from Caucasian origin (MDA-MB-231), and another one was derived from an African American origin (MDA-MB-468). The apoptotic effect of RA was performed using An Annexin V-FITC Apoptosis Detection Kit, while the Propidium Iodide Flow Cytometry Kit was used to detect the cell cycle distribution. Gene expression profiling was established using Human Apoptosis PCR array. The results obtained show that RA significantly caused cytotoxic and antiproliferative effects in both cell lines in a dose- and time-dependent manner. It was noted that RA induced cell cycle arrest-related apoptosis and altered the expression of many apoptosis-involved genes differently. In MDA...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":9113,"name":"Cell Cycle","url":"https://www.academia.edu/Documents/in/Cell_Cycle"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":1335154,"name":"Propidium Iodide","url":"https://www.academia.edu/Documents/in/Propidium_Iodide"},{"id":3101476,"name":"Annexin","url":"https://www.academia.edu/Documents/in/Annexin"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":45280619,"url":"https://aacrjournals.org/cebp/article/29/12_Supplement/PO-132/181580/Abstract-PO-132-Rosmarinic-acid-induced-apoptosis"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950482"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950482/Effects_of_Diallyl_Trisulfide_on_TNF_%CE%B1_stimulated_Genetically_different_Triple_Negative_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Effects of Diallyl Trisulfide on TNF‐α‐stimulated Genetically different Triple‐Negative Breast Cancer Cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950482/Effects_of_Diallyl_Trisulfide_on_TNF_%CE%B1_stimulated_Genetically_different_Triple_Negative_Breast_Cancer_Cells">Effects of Diallyl Trisulfide on TNF‐α‐stimulated Genetically different Triple‐Negative Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>The FASEB Journal</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950482"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950482"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950482; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950482]").text(description); $(".js-view-count[data-work-id=124950482]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950482; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950482']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950482]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950482,"title":"Effects of Diallyl Trisulfide on TNF‐α‐stimulated Genetically different Triple‐Negative Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Wiley","publication_name":"The FASEB Journal"},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950482/Effects_of_Diallyl_Trisulfide_on_TNF_%CE%B1_stimulated_Genetically_different_Triple_Negative_Breast_Cancer_Cells","translated_internal_url":"","created_at":"2024-10-22T08:29:17.778-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Effects_of_Diallyl_Trisulfide_on_TNF_α_stimulated_Genetically_different_Triple_Negative_Breast_Cancer_Cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":32723,"name":"Angiogenesis","url":"https://www.academia.edu/Documents/in/Angiogenesis"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"},{"id":295234,"name":"Chemokine","url":"https://www.academia.edu/Documents/in/Chemokine"},{"id":1461942,"name":"CCL","url":"https://www.academia.edu/Documents/in/CCL"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950481"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950481/Prognostic_Relevance_of_ZNF844_and_Chr_19p13_2_KRAB_Zinc_Finger_Proteins_in_Clear_Cell_Renal_Carcinoma"><img alt="Research paper thumbnail of Prognostic Relevance of ZNF844 and Chr 19p13.2 KRAB-Zinc Finger Proteins in Clear Cell Renal Carcinoma" class="work-thumbnail" src="https://attachments.academia-assets.com/119081018/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950481/Prognostic_Relevance_of_ZNF844_and_Chr_19p13_2_KRAB_Zinc_Finger_Proteins_in_Clear_Cell_Renal_Carcinoma">Prognostic Relevance of ZNF844 and Chr 19p13.2 KRAB-Zinc Finger Proteins in Clear Cell Renal Carcinoma</a></div><div class="wp-workCard_item"><span>Cancer Genomics - Proteomics</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background/Aim: Clear-cell renal cell carcinoma (ccRCC) is the most common and aggressive form of...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background/Aim: Clear-cell renal cell carcinoma (ccRCC) is the most common and aggressive form of all urological cancers, with poor prognosis and high mortality. Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. KRAB Zinc finger proteins (KRAB-ZFPs) are the largest family of mammalian transcription regulators. They are differentially expressed in various tissues during cellular development and phenotypic differentiation. Materials and Methods: In this study, the levels of transcripts of ccRCC from The Cancer Genome Atlas (TCGA) dataset were used to identify prognostic biomarkers in this disease. Results: Using bioinformatics techniques, we demonstrate that approximately 60% of KRAB zinc finger proteins located on chromosome 19p13.2 are differentially expressed, with all but two being down-regulated in ccRCC. Moreover, ZNF844, a paralog of ZNF433, was the most down-regulated across all histological grades and pathological stages (p<0.001). In addition, the decrease in ZNF844 expression was associated with poor patient survival (HR=0.41; 95% CI=0.3-0.56; p<0.0001). Gene Set Enrichment Analysis of genes inversely co-expressed with ZNF844 revealed that enriched pathways were consistently related to immune and translation processes (p<0.05, FDR <0.05). Lastly, ZNF844 expression showed moderate, inverse correlation to Helper Tcell (CD4 or Th1) subtype 1 (R=-0.558, p=5.15×10-39) infiltration and with the exhausted T-cell phenotype (R=-0.37; p=4.1×10-21). Conclusion: Down-regulation of KRAB-ZFPs at 19p13.2 may represent a signature for ccRCC. Moreover, ZNF844 is a prognostic marker for ccRCC and may serve as a putative immune-related tumor suppressor gene. Clear cell renal carcinoma (ccRCC) is the most common neoplastic disease affecting the kidneys. It accounts for at least 70% of all kidney cancers (1, 2). In advanced stages, ccRCC becomes resistant to conventional therapies (1-3). Moreover, later stages are associated with poor prognosis with a 5-year overall survival rate of less than 10% (1-3). Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. Kruppel-associated box domain-containing zinc-finger proteins (KRAB-ZFP) represent the most prominent family of transcriptional repressors (4, 5). The human genome contains over 300 KRAB-ZFPs genes that produce more than 800 transcripts that encode proteins, pseudogenes, and splice variants (6-8). KRAB-ZFPs are differentially expressed in various tissues during cellular development. Several of these genes are involved in embryogenesis, genome imprinting, and biological processes that determine phenotypes in stem cells (9-11). Given their roles in cellular differentiation and their ability to alter gene expression via epigenetic processes and chromatin remodeling, it is conceivable that dysregulation of KRAB-ZFP transcription factors could facilitate tumorigenesis and tumor progression. Interestingly, several large KRAB-ZFP clusters are located on chromosome 19 (chr19), and several studies have linked genetic alterations in chromosome 19p13 to cancers (12-18). Using data mining techniques, we recently identified ZNF433, a zinc finger that is differentially expressed in ccRCC (19) and that may be a biomarker for ccRCC. ZNF433 is part of a cluster of KRAB-ZFPs that are located on chromosome 19p13.2. Thus, we focused on this locus to ascertain if the expression of other members of this cluster was altered. We have identified several KRAB-ZFPs that are differentially expressed and are associated with changes in overall survival in patients. Since the gene ZNF844 is a paralog of ZNF433, it appears to be a strong candidate biomarker and prognostic factor for ccRCC. 305</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="cc8cab3d0a99851de4db3c74eaa79c04" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081018,"asset_id":124950481,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081018/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950481"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950481"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950481; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950481]").text(description); $(".js-view-count[data-work-id=124950481]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950481; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950481']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "cc8cab3d0a99851de4db3c74eaa79c04" } } $('.js-work-strip[data-work-id=124950481]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950481,"title":"Prognostic Relevance of ZNF844 and Chr 19p13.2 KRAB-Zinc Finger Proteins in Clear Cell Renal Carcinoma","translated_title":"","metadata":{"publisher":"Anticancer Research USA Inc.","grobid_abstract":"Background/Aim: Clear-cell renal cell carcinoma (ccRCC) is the most common and aggressive form of all urological cancers, with poor prognosis and high mortality. Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. KRAB Zinc finger proteins (KRAB-ZFPs) are the largest family of mammalian transcription regulators. They are differentially expressed in various tissues during cellular development and phenotypic differentiation. Materials and Methods: In this study, the levels of transcripts of ccRCC from The Cancer Genome Atlas (TCGA) dataset were used to identify prognostic biomarkers in this disease. Results: Using bioinformatics techniques, we demonstrate that approximately 60% of KRAB zinc finger proteins located on chromosome 19p13.2 are differentially expressed, with all but two being down-regulated in ccRCC. Moreover, ZNF844, a paralog of ZNF433, was the most down-regulated across all histological grades and pathological stages (p\u003c0.001). In addition, the decrease in ZNF844 expression was associated with poor patient survival (HR=0.41; 95% CI=0.3-0.56; p\u003c0.0001). Gene Set Enrichment Analysis of genes inversely co-expressed with ZNF844 revealed that enriched pathways were consistently related to immune and translation processes (p\u003c0.05, FDR \u003c0.05). Lastly, ZNF844 expression showed moderate, inverse correlation to Helper Tcell (CD4 or Th1) subtype 1 (R=-0.558, p=5.15×10-39) infiltration and with the exhausted T-cell phenotype (R=-0.37; p=4.1×10-21). Conclusion: Down-regulation of KRAB-ZFPs at 19p13.2 may represent a signature for ccRCC. Moreover, ZNF844 is a prognostic marker for ccRCC and may serve as a putative immune-related tumor suppressor gene. Clear cell renal carcinoma (ccRCC) is the most common neoplastic disease affecting the kidneys. It accounts for at least 70% of all kidney cancers (1, 2). In advanced stages, ccRCC becomes resistant to conventional therapies (1-3). Moreover, later stages are associated with poor prognosis with a 5-year overall survival rate of less than 10% (1-3). Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. Kruppel-associated box domain-containing zinc-finger proteins (KRAB-ZFP) represent the most prominent family of transcriptional repressors (4, 5). The human genome contains over 300 KRAB-ZFPs genes that produce more than 800 transcripts that encode proteins, pseudogenes, and splice variants (6-8). KRAB-ZFPs are differentially expressed in various tissues during cellular development. Several of these genes are involved in embryogenesis, genome imprinting, and biological processes that determine phenotypes in stem cells (9-11). Given their roles in cellular differentiation and their ability to alter gene expression via epigenetic processes and chromatin remodeling, it is conceivable that dysregulation of KRAB-ZFP transcription factors could facilitate tumorigenesis and tumor progression. Interestingly, several large KRAB-ZFP clusters are located on chromosome 19 (chr19), and several studies have linked genetic alterations in chromosome 19p13 to cancers (12-18). Using data mining techniques, we recently identified ZNF433, a zinc finger that is differentially expressed in ccRCC (19) and that may be a biomarker for ccRCC. ZNF433 is part of a cluster of KRAB-ZFPs that are located on chromosome 19p13.2. Thus, we focused on this locus to ascertain if the expression of other members of this cluster was altered. We have identified several KRAB-ZFPs that are differentially expressed and are associated with changes in overall survival in patients. Since the gene ZNF844 is a paralog of ZNF433, it appears to be a strong candidate biomarker and prognostic factor for ccRCC. 305","publication_name":"Cancer Genomics - Proteomics","grobid_abstract_attachment_id":119081018},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950481/Prognostic_Relevance_of_ZNF844_and_Chr_19p13_2_KRAB_Zinc_Finger_Proteins_in_Clear_Cell_Renal_Carcinoma","translated_internal_url":"","created_at":"2024-10-22T08:29:17.497-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081018,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081018/thumbnails/1.jpg","file_name":"305.full.pdf","download_url":"https://www.academia.edu/attachments/119081018/download_file","bulk_download_file_name":"Prognostic_Relevance_of_ZNF844_and_Chr_1.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081018/305.full-libre.pdf?1729611567=\u0026response-content-disposition=attachment%3B+filename%3DPrognostic_Relevance_of_ZNF844_and_Chr_1.pdf\u0026Expires=1742120023\u0026Signature=WmWPVa4IHkvH6takCTGYu8MogJoEi6X0EO40AWBEBXZuaXAlecN3RVy~QNfHN~mlRXGtzNi8jMuwwtvg7rHmUOgvmuWlae4l4W8L-pSQRICRQiyrChoJe34BeTsjrLkNu6MaeBsQ7tB65E~GZJ3gO0viFD~ixC2rv1CwZ~qZpKVF6ZjkKD60GsoMWSHS80RW5cuy86xfJCxJz0LCM0uGW-uSABTecI4oYYsil4B9XXG4hCO3S3c7vRebgReSoOwPmDnxn17U6nkaJRwyw9ystpi19vxIGyVeVDZn9fjotAcEdx7HhAFmAaR4QvtmjEODX4kg~eP7wDp6BNNgbOFMFA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Prognostic_Relevance_of_ZNF844_and_Chr_19p13_2_KRAB_Zinc_Finger_Proteins_in_Clear_Cell_Renal_Carcinoma","translated_slug":"","page_count":23,"language":"en","content_type":"Work","summary":"Background/Aim: Clear-cell renal cell carcinoma (ccRCC) is the most common and aggressive form of all urological cancers, with poor prognosis and high mortality. Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. KRAB Zinc finger proteins (KRAB-ZFPs) are the largest family of mammalian transcription regulators. They are differentially expressed in various tissues during cellular development and phenotypic differentiation. Materials and Methods: In this study, the levels of transcripts of ccRCC from The Cancer Genome Atlas (TCGA) dataset were used to identify prognostic biomarkers in this disease. Results: Using bioinformatics techniques, we demonstrate that approximately 60% of KRAB zinc finger proteins located on chromosome 19p13.2 are differentially expressed, with all but two being down-regulated in ccRCC. Moreover, ZNF844, a paralog of ZNF433, was the most down-regulated across all histological grades and pathological stages (p\u003c0.001). In addition, the decrease in ZNF844 expression was associated with poor patient survival (HR=0.41; 95% CI=0.3-0.56; p\u003c0.0001). Gene Set Enrichment Analysis of genes inversely co-expressed with ZNF844 revealed that enriched pathways were consistently related to immune and translation processes (p\u003c0.05, FDR \u003c0.05). Lastly, ZNF844 expression showed moderate, inverse correlation to Helper Tcell (CD4 or Th1) subtype 1 (R=-0.558, p=5.15×10-39) infiltration and with the exhausted T-cell phenotype (R=-0.37; p=4.1×10-21). Conclusion: Down-regulation of KRAB-ZFPs at 19p13.2 may represent a signature for ccRCC. Moreover, ZNF844 is a prognostic marker for ccRCC and may serve as a putative immune-related tumor suppressor gene. Clear cell renal carcinoma (ccRCC) is the most common neoplastic disease affecting the kidneys. It accounts for at least 70% of all kidney cancers (1, 2). In advanced stages, ccRCC becomes resistant to conventional therapies (1-3). Moreover, later stages are associated with poor prognosis with a 5-year overall survival rate of less than 10% (1-3). Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. Kruppel-associated box domain-containing zinc-finger proteins (KRAB-ZFP) represent the most prominent family of transcriptional repressors (4, 5). The human genome contains over 300 KRAB-ZFPs genes that produce more than 800 transcripts that encode proteins, pseudogenes, and splice variants (6-8). KRAB-ZFPs are differentially expressed in various tissues during cellular development. Several of these genes are involved in embryogenesis, genome imprinting, and biological processes that determine phenotypes in stem cells (9-11). Given their roles in cellular differentiation and their ability to alter gene expression via epigenetic processes and chromatin remodeling, it is conceivable that dysregulation of KRAB-ZFP transcription factors could facilitate tumorigenesis and tumor progression. Interestingly, several large KRAB-ZFP clusters are located on chromosome 19 (chr19), and several studies have linked genetic alterations in chromosome 19p13 to cancers (12-18). Using data mining techniques, we recently identified ZNF433, a zinc finger that is differentially expressed in ccRCC (19) and that may be a biomarker for ccRCC. ZNF433 is part of a cluster of KRAB-ZFPs that are located on chromosome 19p13.2. Thus, we focused on this locus to ascertain if the expression of other members of this cluster was altered. We have identified several KRAB-ZFPs that are differentially expressed and are associated with changes in overall survival in patients. Since the gene ZNF844 is a paralog of ZNF433, it appears to be a strong candidate biomarker and prognostic factor for ccRCC. 305","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081018,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081018/thumbnails/1.jpg","file_name":"305.full.pdf","download_url":"https://www.academia.edu/attachments/119081018/download_file","bulk_download_file_name":"Prognostic_Relevance_of_ZNF844_and_Chr_1.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081018/305.full-libre.pdf?1729611567=\u0026response-content-disposition=attachment%3B+filename%3DPrognostic_Relevance_of_ZNF844_and_Chr_1.pdf\u0026Expires=1742120023\u0026Signature=WmWPVa4IHkvH6takCTGYu8MogJoEi6X0EO40AWBEBXZuaXAlecN3RVy~QNfHN~mlRXGtzNi8jMuwwtvg7rHmUOgvmuWlae4l4W8L-pSQRICRQiyrChoJe34BeTsjrLkNu6MaeBsQ7tB65E~GZJ3gO0viFD~ixC2rv1CwZ~qZpKVF6ZjkKD60GsoMWSHS80RW5cuy86xfJCxJz0LCM0uGW-uSABTecI4oYYsil4B9XXG4hCO3S3c7vRebgReSoOwPmDnxn17U6nkaJRwyw9ystpi19vxIGyVeVDZn9fjotAcEdx7HhAFmAaR4QvtmjEODX4kg~eP7wDp6BNNgbOFMFA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":1290,"name":"Immunology","url":"https://www.academia.edu/Documents/in/Immunology"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":105308,"name":"Renal cell Carcinoma","url":"https://www.academia.edu/Documents/in/Renal_cell_Carcinoma"},{"id":201737,"name":"Clear Cell Renal Cell Carcinoma","url":"https://www.academia.edu/Documents/in/Clear_Cell_Renal_Cell_Carcinoma"},{"id":213897,"name":"Phenotype","url":"https://www.academia.edu/Documents/in/Phenotype"},{"id":213901,"name":"Transcription Factor","url":"https://www.academia.edu/Documents/in/Transcription_Factor"},{"id":329425,"name":"Zinc Finger","url":"https://www.academia.edu/Documents/in/Zinc_Finger"},{"id":340262,"name":"Carcinogenesis","url":"https://www.academia.edu/Documents/in/Carcinogenesis"}],"urls":[{"id":45280618,"url":"https://syndication.highwire.org/content/doi/10.21873/cgp.20322"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950480"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950480/Anaerobic_glycolysis_and_ATP_production_after_complex_I_inhibition_by_MPP_in_C_6_glioma_cells"><img alt="Research paper thumbnail of Anaerobic glycolysis and ATP production after complex I inhibition by MPP+ in C‐6 glioma cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950480/Anaerobic_glycolysis_and_ATP_production_after_complex_I_inhibition_by_MPP_in_C_6_glioma_cells">Anaerobic glycolysis and ATP production after complex I inhibition by MPP+ in C‐6 glioma cells</a></div><div class="wp-workCard_item"><span>The FASEB Journal</span><span>, 2006</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950480"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950480"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950480; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950480]").text(description); $(".js-view-count[data-work-id=124950480]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950480; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950480']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950480]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950480,"title":"Anaerobic glycolysis and ATP production after complex I inhibition by MPP+ in C‐6 glioma cells","translated_title":"","metadata":{"publisher":"Wiley","publication_date":{"day":null,"month":null,"year":2006,"errors":{}},"publication_name":"The FASEB Journal"},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950480/Anaerobic_glycolysis_and_ATP_production_after_complex_I_inhibition_by_MPP_in_C_6_glioma_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:17.298-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Anaerobic_glycolysis_and_ATP_production_after_complex_I_inhibition_by_MPP_in_C_6_glioma_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":61714,"name":"Production economics","url":"https://www.academia.edu/Documents/in/Production_economics"},{"id":76383,"name":"Glioma","url":"https://www.academia.edu/Documents/in/Glioma"},{"id":172897,"name":"Glycolysis","url":"https://www.academia.edu/Documents/in/Glycolysis"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":389302,"name":"Anaerobic Exercise","url":"https://www.academia.edu/Documents/in/Anaerobic_Exercise"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2761404,"name":"anaerobic glycolysis","url":"https://www.academia.edu/Documents/in/anaerobic_glycolysis"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950479"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950479/Hypoxia_Hyperoxia_or_pH_Predominant_Factors_in_Tumor_Cell_Survival"><img alt="Research paper thumbnail of Hypoxia, Hyperoxia or pH ? Predominant Factors in Tumor Cell Survival" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950479/Hypoxia_Hyperoxia_or_pH_Predominant_Factors_in_Tumor_Cell_Survival">Hypoxia, Hyperoxia or pH ? Predominant Factors in Tumor Cell Survival</a></div><div class="wp-workCard_item"><span>The FASEB Journal</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experi...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experimental conditions that do not control for the shift in pH.MethodsHere, we examine the molecular genetic effects of (~91% O2 (hyperoxia) vs. ~2.5% O2 (hypoxia)) at a uniform pH ~7.2 using microarrays, HPLC, imaging probes and Western blot.ResultsHyperoxic and Hypoxic culture conditions for 24 hrs had no adverse effect on viability in malignant N2a cells, provided pH was neutral with ample glucose supply. The hyperoxic transcriptome showed elevation of mRNA of 42 mitochondrial genes, DNA/base excision repair, G protein signaling, protein synthesis, transcription and ubiquitin‐mediated proteolysis. The hypoxic transcriptome corresponded to major elevations in epigenetic (lysine (K)‐specific demethylases, H4k/d/j, Hist4h4, Hist2h3c1, Rara and REST corepressor 2) with greater expression of protein/mRNA for solute carrier family 16, member 3 MCT‐4 (lactate transporter). Blocking MCT‐4 (phloret...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950479"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950479"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950479; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950479]").text(description); $(".js-view-count[data-work-id=124950479]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950479; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950479']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950479]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950479,"title":"Hypoxia, Hyperoxia or pH ? Predominant Factors in Tumor Cell Survival","translated_title":"","metadata":{"abstract":"BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experimental conditions that do not control for the shift in pH.MethodsHere, we examine the molecular genetic effects of (~91% O2 (hyperoxia) vs. ~2.5% O2 (hypoxia)) at a uniform pH ~7.2 using microarrays, HPLC, imaging probes and Western blot.ResultsHyperoxic and Hypoxic culture conditions for 24 hrs had no adverse effect on viability in malignant N2a cells, provided pH was neutral with ample glucose supply. The hyperoxic transcriptome showed elevation of mRNA of 42 mitochondrial genes, DNA/base excision repair, G protein signaling, protein synthesis, transcription and ubiquitin‐mediated proteolysis. The hypoxic transcriptome corresponded to major elevations in epigenetic (lysine (K)‐specific demethylases, H4k/d/j, Hist4h4, Hist2h3c1, Rara and REST corepressor 2) with greater expression of protein/mRNA for solute carrier family 16, member 3 MCT‐4 (lactate transporter). Blocking MCT‐4 (phloret...","publisher":"Wiley","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"The FASEB Journal"},"translated_abstract":"BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experimental conditions that do not control for the shift in pH.MethodsHere, we examine the molecular genetic effects of (~91% O2 (hyperoxia) vs. ~2.5% O2 (hypoxia)) at a uniform pH ~7.2 using microarrays, HPLC, imaging probes and Western blot.ResultsHyperoxic and Hypoxic culture conditions for 24 hrs had no adverse effect on viability in malignant N2a cells, provided pH was neutral with ample glucose supply. The hyperoxic transcriptome showed elevation of mRNA of 42 mitochondrial genes, DNA/base excision repair, G protein signaling, protein synthesis, transcription and ubiquitin‐mediated proteolysis. The hypoxic transcriptome corresponded to major elevations in epigenetic (lysine (K)‐specific demethylases, H4k/d/j, Hist4h4, Hist2h3c1, Rara and REST corepressor 2) with greater expression of protein/mRNA for solute carrier family 16, member 3 MCT‐4 (lactate transporter). Blocking MCT‐4 (phloret...","internal_url":"https://www.academia.edu/124950479/Hypoxia_Hyperoxia_or_pH_Predominant_Factors_in_Tumor_Cell_Survival","translated_internal_url":"","created_at":"2024-10-22T08:29:17.047-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Hypoxia_Hyperoxia_or_pH_Predominant_Factors_in_Tumor_Cell_Survival","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experimental conditions that do not control for the shift in pH.MethodsHere, we examine the molecular genetic effects of (~91% O2 (hyperoxia) vs. ~2.5% O2 (hypoxia)) at a uniform pH ~7.2 using microarrays, HPLC, imaging probes and Western blot.ResultsHyperoxic and Hypoxic culture conditions for 24 hrs had no adverse effect on viability in malignant N2a cells, provided pH was neutral with ample glucose supply. The hyperoxic transcriptome showed elevation of mRNA of 42 mitochondrial genes, DNA/base excision repair, G protein signaling, protein synthesis, transcription and ubiquitin‐mediated proteolysis. The hypoxic transcriptome corresponded to major elevations in epigenetic (lysine (K)‐specific demethylases, H4k/d/j, Hist4h4, Hist2h3c1, Rara and REST corepressor 2) with greater expression of protein/mRNA for solute carrier family 16, member 3 MCT‐4 (lactate transporter). Blocking MCT‐4 (phloret...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":2513,"name":"Molecular Biology","url":"https://www.academia.edu/Documents/in/Molecular_Biology"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":43761,"name":"Transcriptome","url":"https://www.academia.edu/Documents/in/Transcriptome"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":995532,"name":"Hyperoxia","url":"https://www.academia.edu/Documents/in/Hyperoxia"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950478"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950478/Cocaine_potentiates_an_inflammatory_response_in_C6_astroglia_like_cells"><img alt="Research paper thumbnail of Cocaine potentiates an inflammatory response in C6 astroglia‑like cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081012/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950478/Cocaine_potentiates_an_inflammatory_response_in_C6_astroglia_like_cells">Cocaine potentiates an inflammatory response in C6 astroglia‑like cells</a></div><div class="wp-workCard_item"><span>Biomedical Reports</span><span>, 2021</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">cells at higher cocaine doses compared with the unchallenged cells. Since high concentrations of ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">cells at higher cocaine doses compared with the unchallenged cells. Since high concentrations of NO are associated with inflammation, the high levels of NO production observed in the present study suggested that cocaine may have potentiated the inflammatory response in the challenged C6 astroglia-like cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7e6cf18923902df8b053cd1db455c979" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081012,"asset_id":124950478,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081012/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950478"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950478"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950478; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950478]").text(description); $(".js-view-count[data-work-id=124950478]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950478; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950478']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "7e6cf18923902df8b053cd1db455c979" } } $('.js-work-strip[data-work-id=124950478]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950478,"title":"Cocaine potentiates an inflammatory response in C6 astroglia‑like cells","translated_title":"","metadata":{"publisher":"Spandidos Publications","grobid_abstract":"cells at higher cocaine doses compared with the unchallenged cells. Since high concentrations of NO are associated with inflammation, the high levels of NO production observed in the present study suggested that cocaine may have potentiated the inflammatory response in the challenged C6 astroglia-like cells.","publication_date":{"day":null,"month":null,"year":2021,"errors":{}},"publication_name":"Biomedical Reports","grobid_abstract_attachment_id":119081012},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950478/Cocaine_potentiates_an_inflammatory_response_in_C6_astroglia_like_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:16.684-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081012,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081012/thumbnails/1.jpg","file_name":"download.pdf","download_url":"https://www.academia.edu/attachments/119081012/download_file","bulk_download_file_name":"Cocaine_potentiates_an_inflammatory_resp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081012/download-libre.pdf?1729611323=\u0026response-content-disposition=attachment%3B+filename%3DCocaine_potentiates_an_inflammatory_resp.pdf\u0026Expires=1742120023\u0026Signature=NfwKGXH3K2JBK~VFCgRUCBLlS9nCKngORutSOSfyZYIAEYRuYb3O7zRy1T8kZ5WSKnBfqvsjT8rJqE9S4r2dW~nN9MPdkUdgpx---DSKo~QMrMDFjU-cdmuQDHP-vMt-1dC9D176ZU5uYUkpLSzXi4HfViEE~VEsZpBF4IQCUE1TEaE1BKnGfQKdYHw6ECghA97zkbPPyQ-s8KciNrj62p83VBV1qaROYlHUD4ibVh0GGIC~41VfGL-RvfgtwClcWE13aRm~2qy5hHwOb6TA9CEtjr4lTDjxl3GShEuWBz2kdbwbrOIbNbEVLHeISk8NoDhUc1FY~5M5IsnNlr3okQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Cocaine_potentiates_an_inflammatory_response_in_C6_astroglia_like_cells","translated_slug":"","page_count":7,"language":"en","content_type":"Work","summary":"cells at higher cocaine doses compared with the unchallenged cells. Since high concentrations of NO are associated with inflammation, the high levels of NO production observed in the present study suggested that cocaine may have potentiated the inflammatory response in the challenged C6 astroglia-like cells.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081012,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081012/thumbnails/1.jpg","file_name":"download.pdf","download_url":"https://www.academia.edu/attachments/119081012/download_file","bulk_download_file_name":"Cocaine_potentiates_an_inflammatory_resp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081012/download-libre.pdf?1729611323=\u0026response-content-disposition=attachment%3B+filename%3DCocaine_potentiates_an_inflammatory_resp.pdf\u0026Expires=1742120023\u0026Signature=NfwKGXH3K2JBK~VFCgRUCBLlS9nCKngORutSOSfyZYIAEYRuYb3O7zRy1T8kZ5WSKnBfqvsjT8rJqE9S4r2dW~nN9MPdkUdgpx---DSKo~QMrMDFjU-cdmuQDHP-vMt-1dC9D176ZU5uYUkpLSzXi4HfViEE~VEsZpBF4IQCUE1TEaE1BKnGfQKdYHw6ECghA97zkbPPyQ-s8KciNrj62p83VBV1qaROYlHUD4ibVh0GGIC~41VfGL-RvfgtwClcWE13aRm~2qy5hHwOb6TA9CEtjr4lTDjxl3GShEuWBz2kdbwbrOIbNbEVLHeISk8NoDhUc1FY~5M5IsnNlr3okQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":140,"name":"Pharmacology","url":"https://www.academia.edu/Documents/in/Pharmacology"},{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":48183,"name":"Lipopolysaccharide","url":"https://www.academia.edu/Documents/in/Lipopolysaccharide"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950477"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950477/Effect_of_Diallyl_Trisulfide_on_TNF_%CE%B1_induced_CCL2_MCP_1_Release_in_Genetically_Different_Triple_negative_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081015/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950477/Effect_of_Diallyl_Trisulfide_on_TNF_%CE%B1_induced_CCL2_MCP_1_Release_in_Genetically_Different_Triple_negative_Breast_Cancer_Cells">Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>Anticancer Research</span><span>, 2021</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit breast carcinogen...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit breast carcinogenesis. CCL2/MCP-1 has been shown to play a significant role in breast cancer. This study explored DATS efficacy on triple-negative breast cancer (TNBC) cells. Materials and Methods: DATS efficacy on TNFα induced TNBC cells were examined via trypan blue exclusion test, wound-healing assay, human cytokine arrays, ELISA, and RT-PCR. Results: DATS significantly induced cell death and inhibited cell migration. Expression of CCL2/MCP-1, IL-6, PDGF-BB, NT-3, and GM-CSF in TNF-α-treated cells increased. However, DATS significantly decreased the expression of CCL2/MCP-1 in TNF-α-treated MDA-MB-231 but not in MDA-MB-468 cells. DATS significantly down-regulated mRNA expression of IKBKE and MAPK8 in both cell lines, indicating a possible effect in genes involved in the NF-ĸB and MAPK signaling. Conclusion: DATS may have a role in TNBC therapy and prevention by targeting CCL2.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f57cd9a30ef121ff634af43a91426ab7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081015,"asset_id":124950477,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081015/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950477"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950477"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950477; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950477]").text(description); $(".js-view-count[data-work-id=124950477]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950477; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950477']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "f57cd9a30ef121ff634af43a91426ab7" } } $('.js-work-strip[data-work-id=124950477]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950477,"title":"Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Anticancer Research USA Inc.","grobid_abstract":"Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit breast carcinogenesis. CCL2/MCP-1 has been shown to play a significant role in breast cancer. This study explored DATS efficacy on triple-negative breast cancer (TNBC) cells. Materials and Methods: DATS efficacy on TNFα induced TNBC cells were examined via trypan blue exclusion test, wound-healing assay, human cytokine arrays, ELISA, and RT-PCR. Results: DATS significantly induced cell death and inhibited cell migration. Expression of CCL2/MCP-1, IL-6, PDGF-BB, NT-3, and GM-CSF in TNF-α-treated cells increased. However, DATS significantly decreased the expression of CCL2/MCP-1 in TNF-α-treated MDA-MB-231 but not in MDA-MB-468 cells. DATS significantly down-regulated mRNA expression of IKBKE and MAPK8 in both cell lines, indicating a possible effect in genes involved in the NF-ĸB and MAPK signaling. Conclusion: DATS may have a role in TNBC therapy and prevention by targeting CCL2.","publication_date":{"day":null,"month":null,"year":2021,"errors":{}},"publication_name":"Anticancer Research","grobid_abstract_attachment_id":119081015},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950477/Effect_of_Diallyl_Trisulfide_on_TNF_%CE%B1_induced_CCL2_MCP_1_Release_in_Genetically_Different_Triple_negative_Breast_Cancer_Cells","translated_internal_url":"","created_at":"2024-10-22T08:29:16.439-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081015,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081015/thumbnails/1.jpg","file_name":"5919.full.pdf","download_url":"https://www.academia.edu/attachments/119081015/download_file","bulk_download_file_name":"Effect_of_Diallyl_Trisulfide_on_TNF__in.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081015/5919.full-libre.pdf?1729611354=\u0026response-content-disposition=attachment%3B+filename%3DEffect_of_Diallyl_Trisulfide_on_TNF__in.pdf\u0026Expires=1742120023\u0026Signature=ch3H9S4TLVr~b-Qa5M53PyW19UZZ6pV4URTR1KHDtM9jMzck3kwcTy6AvseF5vFhGQnfiBAg8H2MvXKvMwSD9xkC1qOwYxcLXTVbIuLEDBaD8xmfHfFF5nwP0hN9UqucaDL0A1P7W1QsX-sP18fQbA8~h3YHi1bT4g5WUgWpp9cT~f2QD3x5nzOnYoojUP-4dw86URpBD6phdICkVVSgYSMp53h6N8XfOzn71NVsr7VBDdzh4euqnaws5XyE0MXu9LWCVQ1ZrQL5cEPawoDLinroanvaNx-1mH3wm2dRUvaptZddi~SjpD7qNpHv-K80OgIw2Ht~sPlp4Ecga7DDaQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Effect_of_Diallyl_Trisulfide_on_TNF_α_induced_CCL2_MCP_1_Release_in_Genetically_Different_Triple_negative_Breast_Cancer_Cells","translated_slug":"","page_count":15,"language":"en","content_type":"Work","summary":"Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit breast carcinogenesis. CCL2/MCP-1 has been shown to play a significant role in breast cancer. This study explored DATS efficacy on triple-negative breast cancer (TNBC) cells. Materials and Methods: DATS efficacy on TNFα induced TNBC cells were examined via trypan blue exclusion test, wound-healing assay, human cytokine arrays, ELISA, and RT-PCR. Results: DATS significantly induced cell death and inhibited cell migration. Expression of CCL2/MCP-1, IL-6, PDGF-BB, NT-3, and GM-CSF in TNF-α-treated cells increased. However, DATS significantly decreased the expression of CCL2/MCP-1 in TNF-α-treated MDA-MB-231 but not in MDA-MB-468 cells. DATS significantly down-regulated mRNA expression of IKBKE and MAPK8 in both cell lines, indicating a possible effect in genes involved in the NF-ĸB and MAPK signaling. Conclusion: DATS may have a role in TNBC therapy and prevention by targeting CCL2.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081015,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081015/thumbnails/1.jpg","file_name":"5919.full.pdf","download_url":"https://www.academia.edu/attachments/119081015/download_file","bulk_download_file_name":"Effect_of_Diallyl_Trisulfide_on_TNF__in.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081015/5919.full-libre.pdf?1729611354=\u0026response-content-disposition=attachment%3B+filename%3DEffect_of_Diallyl_Trisulfide_on_TNF__in.pdf\u0026Expires=1742120023\u0026Signature=ch3H9S4TLVr~b-Qa5M53PyW19UZZ6pV4URTR1KHDtM9jMzck3kwcTy6AvseF5vFhGQnfiBAg8H2MvXKvMwSD9xkC1qOwYxcLXTVbIuLEDBaD8xmfHfFF5nwP0hN9UqucaDL0A1P7W1QsX-sP18fQbA8~h3YHi1bT4g5WUgWpp9cT~f2QD3x5nzOnYoojUP-4dw86URpBD6phdICkVVSgYSMp53h6N8XfOzn71NVsr7VBDdzh4euqnaws5XyE0MXu9LWCVQ1ZrQL5cEPawoDLinroanvaNx-1mH3wm2dRUvaptZddi~SjpD7qNpHv-K80OgIw2Ht~sPlp4Ecga7DDaQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":263843,"name":"Anticancer","url":"https://www.academia.edu/Documents/in/Anticancer"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"},{"id":376275,"name":"Trypan Blue","url":"https://www.academia.edu/Documents/in/Trypan_Blue"},{"id":474029,"name":"Tumor necrosis factor-alpha","url":"https://www.academia.edu/Documents/in/Tumor_necrosis_factor-alpha"},{"id":1461942,"name":"CCL","url":"https://www.academia.edu/Documents/in/CCL"}],"urls":[{"id":45280617,"url":"https://syndication.highwire.org/content/doi/10.21873/anticanres.15411"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950476"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950476/Epigenetic_Patterns_Therapies_Associated_with_Genetic_Disorders"><img alt="Research paper thumbnail of Epigenetic Patterns/Therapies Associated with Genetic Disorders" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950476/Epigenetic_Patterns_Therapies_Associated_with_Genetic_Disorders">Epigenetic Patterns/Therapies Associated with Genetic Disorders</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Within the past three centuries, all-cause disease burden in developed countries has shifted from...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Within the past three centuries, all-cause disease burden in developed countries has shifted from infectious to non-communicable (NCD)/genetic based diseases including cardiovascular conditions, cancer, neuropsychiatric conditions, and diabetes. Factors accounting for this drift include discoveries in vaccination (e.g., tetanus, cholera, typhoid, plague, anthrax, and tuberculosis), antibiotics, advances in medical diagnostics, lasers, surgical techniques, and routine medicines to treat almost every type of systemic imbalance. Moreover, advances in public health, sanitation, food safety, and geriatric sciences are creating extended life expectancy, where age-related illnesses (osteoarthritis, back pain, neurodegenerative conditions) in addition to NCDs are plaguing an ever-growing elderly population. The age-related risk for these diseases is now worsened by aggregation of global industrial pollutants, where the World Health Organization (WHO) now uses the term “environmental burden ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950476"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950476"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950476; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950476]").text(description); $(".js-view-count[data-work-id=124950476]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950476; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950476']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950476]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950476,"title":"Epigenetic Patterns/Therapies Associated with Genetic Disorders","translated_title":"","metadata":{"abstract":"Within the past three centuries, all-cause disease burden in developed countries has shifted from infectious to non-communicable (NCD)/genetic based diseases including cardiovascular conditions, cancer, neuropsychiatric conditions, and diabetes. Factors accounting for this drift include discoveries in vaccination (e.g., tetanus, cholera, typhoid, plague, anthrax, and tuberculosis), antibiotics, advances in medical diagnostics, lasers, surgical techniques, and routine medicines to treat almost every type of systemic imbalance. Moreover, advances in public health, sanitation, food safety, and geriatric sciences are creating extended life expectancy, where age-related illnesses (osteoarthritis, back pain, neurodegenerative conditions) in addition to NCDs are plaguing an ever-growing elderly population. The age-related risk for these diseases is now worsened by aggregation of global industrial pollutants, where the World Health Organization (WHO) now uses the term “environmental burden ...","publication_date":{"day":null,"month":null,"year":2018,"errors":{}}},"translated_abstract":"Within the past three centuries, all-cause disease burden in developed countries has shifted from infectious to non-communicable (NCD)/genetic based diseases including cardiovascular conditions, cancer, neuropsychiatric conditions, and diabetes. Factors accounting for this drift include discoveries in vaccination (e.g., tetanus, cholera, typhoid, plague, anthrax, and tuberculosis), antibiotics, advances in medical diagnostics, lasers, surgical techniques, and routine medicines to treat almost every type of systemic imbalance. Moreover, advances in public health, sanitation, food safety, and geriatric sciences are creating extended life expectancy, where age-related illnesses (osteoarthritis, back pain, neurodegenerative conditions) in addition to NCDs are plaguing an ever-growing elderly population. The age-related risk for these diseases is now worsened by aggregation of global industrial pollutants, where the World Health Organization (WHO) now uses the term “environmental burden ...","internal_url":"https://www.academia.edu/124950476/Epigenetic_Patterns_Therapies_Associated_with_Genetic_Disorders","translated_internal_url":"","created_at":"2024-10-22T08:29:16.203-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Epigenetic_Patterns_Therapies_Associated_with_Genetic_Disorders","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Within the past three centuries, all-cause disease burden in developed countries has shifted from infectious to non-communicable (NCD)/genetic based diseases including cardiovascular conditions, cancer, neuropsychiatric conditions, and diabetes. Factors accounting for this drift include discoveries in vaccination (e.g., tetanus, cholera, typhoid, plague, anthrax, and tuberculosis), antibiotics, advances in medical diagnostics, lasers, surgical techniques, and routine medicines to treat almost every type of systemic imbalance. Moreover, advances in public health, sanitation, food safety, and geriatric sciences are creating extended life expectancy, where age-related illnesses (osteoarthritis, back pain, neurodegenerative conditions) in addition to NCDs are plaguing an ever-growing elderly population. The age-related risk for these diseases is now worsened by aggregation of global industrial pollutants, where the World Health Organization (WHO) now uses the term “environmental burden ...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":99773,"name":"Disease","url":"https://www.academia.edu/Documents/in/Disease"},{"id":172892,"name":"Life Expectancy","url":"https://www.academia.edu/Documents/in/Life_Expectancy"},{"id":3647879,"name":"Springer Ebooks","url":"https://www.academia.edu/Documents/in/Springer_Ebooks"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950475"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950475/Astrocytic_transcription_factor_REST_upregulates_glutamate_transporter_EAAT2_protecting_dopaminergic_neurons_from_manganese_induced_excitotoxicity"><img alt="Research paper thumbnail of Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity" class="work-thumbnail" src="https://attachments.academia-assets.com/119081014/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950475/Astrocytic_transcription_factor_REST_upregulates_glutamate_transporter_EAAT2_protecting_dopaminergic_neurons_from_manganese_induced_excitotoxicity">Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity</a></div><div class="wp-workCard_item"><span>Journal of Biological Chemistry</span><span>, 2021</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="685f2ab236f63d3c50f2f1ca5543f4a0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081014,"asset_id":124950475,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081014/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950475"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950475"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950475; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "685f2ab236f63d3c50f2f1ca5543f4a0" } } $('.js-work-strip[data-work-id=124950475]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950475,"title":"Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity","translated_title":"","metadata":{"publisher":"Elsevier BV","ai_abstract":"Chronic exposure to manganese (Mn) leads to manganism, resembling Parkinson's disease symptoms, with EAAT2 being crucial for maintaining glutamate levels in the brain. This study identifies that the transcription factor REST enhances EAAT2 expression in astrocytes, thus mitigating Mn-induced excitotoxicity in dopaminergic neurons. REST's mechanism involves recruiting epigenetic modifiers to the EAAT2 promoter, presenting it as a potential target for therapeutic strategies against Mn neurotoxicity and related neurological disorders.","ai_title_tag":"REST Enhances EAAT2 to Protect Neurons from Mn","publication_date":{"day":null,"month":null,"year":2021,"errors":{}},"publication_name":"Journal of Biological Chemistry"},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950475/Astrocytic_transcription_factor_REST_upregulates_glutamate_transporter_EAAT2_protecting_dopaminergic_neurons_from_manganese_induced_excitotoxicity","translated_internal_url":"","created_at":"2024-10-22T08:29:15.959-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081014,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081014/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081014/download_file","bulk_download_file_name":"Astrocytic_transcription_factor_REST_upr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081014/pdf-libre.pdf?1729611329=\u0026response-content-disposition=attachment%3B+filename%3DAstrocytic_transcription_factor_REST_upr.pdf\u0026Expires=1742120023\u0026Signature=Nako0vT2FPCKTTN4KcLD-B9GMHzU2oJGF~1vGaPbkClKTskfDu8yf0Nho58sGst2ddiA~KaLzcnuC2CSAXq~UMNC0AQmid2-u3wGG5HrjqK~ubTkaUZRCKQPWbFrl3D5y56c1yqrKqNU45mWAMZ3u7-7A~1uGRzLyhtDyx5Me2izOuCCrM2KFQTRcKLpYdPUBQ0xw~Ww5eD2B6b5cBRSUC8UBSCZyf4UHLUI9M06ZWYvVm~lNut~HWP5PlL3qQZdTHl9ly2OtbbaSsYOpRShgrWTOlwIDo6XkTMPrPbawVs8Mgc6jR~0ie0o5Gws5SEsMVDXms0qozvUCx2dTBH2rw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Astrocytic_transcription_factor_REST_upregulates_glutamate_transporter_EAAT2_protecting_dopaminergic_neurons_from_manganese_induced_excitotoxicity","translated_slug":"","page_count":16,"language":"en","content_type":"Work","summary":null,"owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081014,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081014/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081014/download_file","bulk_download_file_name":"Astrocytic_transcription_factor_REST_upr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081014/pdf-libre.pdf?1729611329=\u0026response-content-disposition=attachment%3B+filename%3DAstrocytic_transcription_factor_REST_upr.pdf\u0026Expires=1742120023\u0026Signature=Nako0vT2FPCKTTN4KcLD-B9GMHzU2oJGF~1vGaPbkClKTskfDu8yf0Nho58sGst2ddiA~KaLzcnuC2CSAXq~UMNC0AQmid2-u3wGG5HrjqK~ubTkaUZRCKQPWbFrl3D5y56c1yqrKqNU45mWAMZ3u7-7A~1uGRzLyhtDyx5Me2izOuCCrM2KFQTRcKLpYdPUBQ0xw~Ww5eD2B6b5cBRSUC8UBSCZyf4UHLUI9M06ZWYvVm~lNut~HWP5PlL3qQZdTHl9ly2OtbbaSsYOpRShgrWTOlwIDo6XkTMPrPbawVs8Mgc6jR~0ie0o5Gws5SEsMVDXms0qozvUCx2dTBH2rw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":18520,"name":"Biological Chemistry","url":"https://www.academia.edu/Documents/in/Biological_Chemistry"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":37851,"name":"Neuroprotection","url":"https://www.academia.edu/Documents/in/Neuroprotection"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":125522,"name":"Neurotoxicity","url":"https://www.academia.edu/Documents/in/Neurotoxicity"},{"id":130116,"name":"Astrocyte","url":"https://www.academia.edu/Documents/in/Astrocyte"},{"id":260118,"name":"CHEMICAL SCIENCES","url":"https://www.academia.edu/Documents/in/CHEMICAL_SCIENCES"},{"id":1151966,"name":"Excitotoxicity","url":"https://www.academia.edu/Documents/in/Excitotoxicity"},{"id":2012816,"name":"Glutamate Receptor","url":"https://www.academia.edu/Documents/in/Glutamate_Receptor"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":45280616,"url":"https://api.elsevier.com/content/article/PII:S0021925821011789?httpAccept=text/xml"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950474"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950474/Molecular_mechanism_of_gossypol_mediating_CCL2_and_IL_8_attenuation_in_triple_negative_breast_cancer_cells"><img alt="Research paper thumbnail of Molecular mechanism of gossypol mediating CCL2 and IL‑8 attenuation in triple‑negative breast cancer cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081013/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950474/Molecular_mechanism_of_gossypol_mediating_CCL2_and_IL_8_attenuation_in_triple_negative_breast_cancer_cells">Molecular mechanism of gossypol mediating CCL2 and IL‑8 attenuation in triple‑negative breast cancer cells</a></div><div class="wp-workCard_item"><span>Molecular Medicine Reports</span><span>, 2020</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">chronic inflammation associated with cancer is characterized by the production of different types...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">chronic inflammation associated with cancer is characterized by the production of different types of chemokines and cytokines. in cancer, numerous signaling pathways upregulate the expression levels of several cytokines and evolve cells to the neoplastic state. Therefore, targeting these signaling pathways through the inhibition of distinctive gene expression is a primary target for cancer therapy. The present study investigated the anticancer effects of the natural polyphenol gossypol (GoSS) in triple-negative breast cancer (TnBc) cells, the most aggressive breast cancer type with poor prognosis. GoSS effects were examined in two TnBc cell lines: Mda-MB-231 (MM-231) and Mda-MB-468 (MM-468), representing caucasian americans (ca) and african americans (aa), respectively. The obtained ic 50 s revealed no significant difference between the two cell lines' response to the compound. However, the use of microarray assays for cytokine determination indicated the ability of GoSS to attenuate the expression levels of cancer-related cytokines in the two cell lines. although GoSS did not alter ccl2 expression in MM-468 cells, it was able to cause 30% inhibition in TnF-α-stimulated MM-231 cells. additionally, il-8 was not altered by GoSS treatment in MM-231 cells, while its expression was inhibited by 60% in TnF-α-activated MM-468 cells. eliSa assays supported the microarray data and indicated that ccl2 expression was inhibited by 40% in MM-231 cells, and il-8 expression was inhibited by 50% in MM-468 cells. Furthermore, in MM-231 cells, GoSS inhibited ccl2 release via the repression of iKBKe, CCL2 and MAPK1 gene expression. additionally, in MM-468 cells, the compound downregulated the release of il-8 through repressing IL-8, MAPK1, MAPK3, CCDC88A, STAT3 and PIK3CD gene expression. in conclusion, the data obtained in the present study indicate that the polyphenol compound GoSS may provide a valuable tool in TnBc therapy.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3f5507352afdff1e7a4292ff1e8a0d67" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081013,"asset_id":124950474,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081013/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950474"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950474"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950474; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950474]").text(description); $(".js-view-count[data-work-id=124950474]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950474; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950474']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "3f5507352afdff1e7a4292ff1e8a0d67" } } $('.js-work-strip[data-work-id=124950474]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950474,"title":"Molecular mechanism of gossypol mediating CCL2 and IL‑8 attenuation in triple‑negative breast cancer cells","translated_title":"","metadata":{"publisher":"Spandidos Publications","ai_title_tag":"Gossypol Reduces CCL2 and IL-8 in Triple-Negative Breast Cancer","grobid_abstract":"chronic inflammation associated with cancer is characterized by the production of different types of chemokines and cytokines. in cancer, numerous signaling pathways upregulate the expression levels of several cytokines and evolve cells to the neoplastic state. Therefore, targeting these signaling pathways through the inhibition of distinctive gene expression is a primary target for cancer therapy. The present study investigated the anticancer effects of the natural polyphenol gossypol (GoSS) in triple-negative breast cancer (TnBc) cells, the most aggressive breast cancer type with poor prognosis. GoSS effects were examined in two TnBc cell lines: Mda-MB-231 (MM-231) and Mda-MB-468 (MM-468), representing caucasian americans (ca) and african americans (aa), respectively. The obtained ic 50 s revealed no significant difference between the two cell lines' response to the compound. However, the use of microarray assays for cytokine determination indicated the ability of GoSS to attenuate the expression levels of cancer-related cytokines in the two cell lines. although GoSS did not alter ccl2 expression in MM-468 cells, it was able to cause 30% inhibition in TnF-α-stimulated MM-231 cells. additionally, il-8 was not altered by GoSS treatment in MM-231 cells, while its expression was inhibited by 60% in TnF-α-activated MM-468 cells. eliSa assays supported the microarray data and indicated that ccl2 expression was inhibited by 40% in MM-231 cells, and il-8 expression was inhibited by 50% in MM-468 cells. Furthermore, in MM-231 cells, GoSS inhibited ccl2 release via the repression of iKBKe, CCL2 and MAPK1 gene expression. additionally, in MM-468 cells, the compound downregulated the release of il-8 through repressing IL-8, MAPK1, MAPK3, CCDC88A, STAT3 and PIK3CD gene expression. in conclusion, the data obtained in the present study indicate that the polyphenol compound GoSS may provide a valuable tool in TnBc therapy.","publication_date":{"day":null,"month":null,"year":2020,"errors":{}},"publication_name":"Molecular Medicine Reports","grobid_abstract_attachment_id":119081013},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950474/Molecular_mechanism_of_gossypol_mediating_CCL2_and_IL_8_attenuation_in_triple_negative_breast_cancer_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:15.771-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081013,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081013/thumbnails/1.jpg","file_name":"download.pdf","download_url":"https://www.academia.edu/attachments/119081013/download_file","bulk_download_file_name":"Molecular_mechanism_of_gossypol_mediatin.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081013/download-libre.pdf?1729611338=\u0026response-content-disposition=attachment%3B+filename%3DMolecular_mechanism_of_gossypol_mediatin.pdf\u0026Expires=1742120023\u0026Signature=WM8rDvL9U05zJALk6Kb0M2EGa5D4LmsUQcmNgTCvUs-LvMAumFhmyej59pz1YuxTn~AAytKKZesz3i-Tuha3yLK~z6iFuPGjRtb~t7wsot8AQTnVViP07NnozifGIdkxd-Nb-Q0TZcHAroNYitsFsm84I5jLTD0s1wqcb-4ptr9EPClu169dK1~Zao7yFJNaRvhIIL9DqGRD89nlwEohsMuDht6lNXxw-pYy33S3m~D3WC5KluWHloh0GF7GzcxYe5OE2jXwilunrJB96gOwhNa600kK2ZsIoyHk9~YlnFnozq81dov7JoEkqYemrqOTMJXBiFTmMA2lHzKOvJEoSw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Molecular_mechanism_of_gossypol_mediating_CCL2_and_IL_8_attenuation_in_triple_negative_breast_cancer_cells","translated_slug":"","page_count":14,"language":"en","content_type":"Work","summary":"chronic inflammation associated with cancer is characterized by the production of different types of chemokines and cytokines. in cancer, numerous signaling pathways upregulate the expression levels of several cytokines and evolve cells to the neoplastic state. Therefore, targeting these signaling pathways through the inhibition of distinctive gene expression is a primary target for cancer therapy. The present study investigated the anticancer effects of the natural polyphenol gossypol (GoSS) in triple-negative breast cancer (TnBc) cells, the most aggressive breast cancer type with poor prognosis. GoSS effects were examined in two TnBc cell lines: Mda-MB-231 (MM-231) and Mda-MB-468 (MM-468), representing caucasian americans (ca) and african americans (aa), respectively. The obtained ic 50 s revealed no significant difference between the two cell lines' response to the compound. However, the use of microarray assays for cytokine determination indicated the ability of GoSS to attenuate the expression levels of cancer-related cytokines in the two cell lines. although GoSS did not alter ccl2 expression in MM-468 cells, it was able to cause 30% inhibition in TnF-α-stimulated MM-231 cells. additionally, il-8 was not altered by GoSS treatment in MM-231 cells, while its expression was inhibited by 60% in TnF-α-activated MM-468 cells. eliSa assays supported the microarray data and indicated that ccl2 expression was inhibited by 40% in MM-231 cells, and il-8 expression was inhibited by 50% in MM-468 cells. Furthermore, in MM-231 cells, GoSS inhibited ccl2 release via the repression of iKBKe, CCL2 and MAPK1 gene expression. additionally, in MM-468 cells, the compound downregulated the release of il-8 through repressing IL-8, MAPK1, MAPK3, CCDC88A, STAT3 and PIK3CD gene expression. in conclusion, the data obtained in the present study indicate that the polyphenol compound GoSS may provide a valuable tool in TnBc therapy.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081013,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081013/thumbnails/1.jpg","file_name":"download.pdf","download_url":"https://www.academia.edu/attachments/119081013/download_file","bulk_download_file_name":"Molecular_mechanism_of_gossypol_mediatin.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081013/download-libre.pdf?1729611338=\u0026response-content-disposition=attachment%3B+filename%3DMolecular_mechanism_of_gossypol_mediatin.pdf\u0026Expires=1742120023\u0026Signature=WM8rDvL9U05zJALk6Kb0M2EGa5D4LmsUQcmNgTCvUs-LvMAumFhmyej59pz1YuxTn~AAytKKZesz3i-Tuha3yLK~z6iFuPGjRtb~t7wsot8AQTnVViP07NnozifGIdkxd-Nb-Q0TZcHAroNYitsFsm84I5jLTD0s1wqcb-4ptr9EPClu169dK1~Zao7yFJNaRvhIIL9DqGRD89nlwEohsMuDht6lNXxw-pYy33S3m~D3WC5KluWHloh0GF7GzcxYe5OE2jXwilunrJB96gOwhNa600kK2ZsIoyHk9~YlnFnozq81dov7JoEkqYemrqOTMJXBiFTmMA2lHzKOvJEoSw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":6021,"name":"Cancer","url":"https://www.academia.edu/Documents/in/Cancer"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":106169,"name":"Oncogene","url":"https://www.academia.edu/Documents/in/Oncogene"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"},{"id":1461942,"name":"CCL","url":"https://www.academia.edu/Documents/in/CCL"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950473"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950473/Identification_of_cytotoxic_markers_in_methamphetamine_treated_rat_C6_astroglia_like_cells"><img alt="Research paper thumbnail of Identification of cytotoxic markers in methamphetamine treated rat C6 astroglia-like cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119080987/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950473/Identification_of_cytotoxic_markers_in_methamphetamine_treated_rat_C6_astroglia_like_cells">Identification of cytotoxic markers in methamphetamine treated rat C6 astroglia-like cells</a></div><div class="wp-workCard_item"><span>Scientific Reports</span><span>, 2019</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Methamphetamine (METH) is a powerfully addictive psychostimulant that has a pronounced effect on ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Methamphetamine (METH) is a powerfully addictive psychostimulant that has a pronounced effect on the central nervous system (CNS). The present study aimed to assess METH toxicity in differentiated C6 astroglia-like cells through biochemical and toxicity markers with acute (1 h) and chronic (48 h) treatments. In the absence of external stimulants, cellular differentiation of neuronal morphology was achieved through reduced serum (2.5%) in the medium. The cells displayed branched neurite-like processes with extensive intercellular connections. Results indicated that acute METH treatment neither altered the cell morphology nor killed the cells, which echoed with lack of consequence on reactive oxygen species (ROS), nitric oxide (NO) or inhibition of any cell cycle phases except induction of cytoplasmic vacuoles. On the other hand, chronic treatment at 1 mM or above destroyed the neurite-like processors and decreased the cell viability that paralleled with increased levels of ROS, lipid...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0586728ee04773ae3a42bf0be79bac62" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119080987,"asset_id":124950473,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119080987/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950473"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950473"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950473; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950473]").text(description); $(".js-view-count[data-work-id=124950473]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950473; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950473']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0586728ee04773ae3a42bf0be79bac62" } } $('.js-work-strip[data-work-id=124950473]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950473,"title":"Identification of cytotoxic markers in methamphetamine treated rat C6 astroglia-like cells","translated_title":"","metadata":{"abstract":"Methamphetamine (METH) is a powerfully addictive psychostimulant that has a pronounced effect on the central nervous system (CNS). 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950472"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950472/The_Research_Centers_in_Minority_Institutions_RCMI_Translational_Research_Network_Building_and_Sustaining_Capacity_for_Multi_Site_Basic_Biomedical_Clinical_and_Behavioral_Research"><img alt="Research paper thumbnail of The Research Centers in Minority Institutions (RCMI) Translational Research Network: Building and Sustaining Capacity for Multi-Site Basic Biomedical, Clinical and Behavioral Research" class="work-thumbnail" src="https://attachments.academia-assets.com/119080986/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950472/The_Research_Centers_in_Minority_Institutions_RCMI_Translational_Research_Network_Building_and_Sustaining_Capacity_for_Multi_Site_Basic_Biomedical_Clinical_and_Behavioral_Research">The Research Centers in Minority Institutions (RCMI) Translational Research Network: Building and Sustaining Capacity for Multi-Site Basic Biomedical, Clinical and Behavioral Research</a></div><div class="wp-workCard_item"><span>Ethnicity & Disease</span><span>, 2019</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The Research Centers in Minority Institutions (RCMI) program was established by the US Congress ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The Research Centers in Minority Institutions (RCMI) program was established by the US Congress to support the development of biomedical research infrastructure at minority-serving institutions granting doctoral degrees in the health professions or in a health-related science. RCMI institutions also conduct research on diseases that disproportionately affect racial and ethnic minorities (ie, African Americans/Blacks, American Indians and Alaska Natives, Hispanics, Native Hawaiians and Other Pacific Islanders), those of low socioeconomic status, and rural persons. Quantitative metrics, including the numbers of doctoral science degrees granted to underrepresented students, NIH peer-reviewed research funding, peer-reviewed publications, and numbers of racial and ethnic minorities participating in sponsored research, demonstrate that RCMI grantee institutions have made substantial progress toward the intent of the Congressional legislation, as well as the NIH/NIMHD-linked goals o...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="dbd852d1096129bdb6d53184736dba0a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119080986,"asset_id":124950472,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119080986/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950472"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950472"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950472; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950472]").text(description); $(".js-view-count[data-work-id=124950472]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950472; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950472']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "dbd852d1096129bdb6d53184736dba0a" } } $('.js-work-strip[data-work-id=124950472]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950472,"title":"The Research Centers in Minority Institutions (RCMI) Translational Research Network: Building and Sustaining Capacity for Multi-Site Basic Biomedical, Clinical and Behavioral Research","translated_title":"","metadata":{"abstract":"The Research Centers in Minority Institutions (RCMI) program was established by the US Congress to support the development of biomedical research infrastructure at minority-serving institutions granting doctoral degrees in the health professions or in a health-related science. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="1032437" id="papers"><div class="js-work-strip profile--work_container" data-work-id="124950491"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950491/Involvement_of_AKT_PI3K_Pathway_in_Sanguinarine_s_Induced_Apoptosis_and_Cell_Cycle_Arrest_in_Triple_negative_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Involvement of AKT/PI3K Pathway in Sanguinarine’s Induced Apoptosis and Cell Cycle Arrest in Triple-negative Breast Cancer Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081022/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950491/Involvement_of_AKT_PI3K_Pathway_in_Sanguinarine_s_Induced_Apoptosis_and_Cell_Cycle_Arrest_in_Triple_negative_Breast_Cancer_Cells">Involvement of AKT/PI3K Pathway in Sanguinarine’s Induced Apoptosis and Cell Cycle Arrest in Triple-negative Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>Cancer Genomics - Proteomics</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background/Aim: Chemotherapy resistance in triple-negative breast cancer (TNBC) cells is well doc...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background/Aim: Chemotherapy resistance in triple-negative breast cancer (TNBC) cells is well documented. Therefore, it is necessary to develop safer and more effective therapeutic agents to enhance the outcomes of chemotherapeutic agents. The natural alkaloid sanguinarine (SANG) has demonstrated therapeutic synergy when coupled with chemotherapeutic agents. SANG can also induce cell cycle arrest and trigger apoptosis in various cancer cells. Materials and Methods: In this study, we investigated the molecular mechanism underlying SANG activity in MDA-MB-231 and MDA-MB-468 cells as two genetically different models of TNBC. We employed various assays including Alamar Blue to measure the effect of SANG on cell viability and proliferation rate, flow cytometry analysis to study the potential of the compound to induce apoptosis and cell cycle arrest, quantitative qRT PCR apoptosis array to measure the expression of different genes mediating apoptosis, and the western system was used to analyze the impact of the compound on AKT protein expression. Results: SANG lowered cell viability and disrupted cell cycle progression in both cell lines. Furthermore, S-phase cell cycle arrest-mediated apoptosis was found to be the primary contributor to cell growth inhibition in MDA-MB-231 cells. SANG-treated TNBC cells showed significantly up-regulated mRNA expression of 18 genes associated with apoptosis, including eight TNF receptor superfamily (TNFRSF), three members of the BCL2 family, and two members of the caspase (CASP) family in MDA-MB-468 cells. In MDA-MB-231 cells, two members of the TNF superfamily and four members of the BCL2 family were affected. The western study data showed the inhibition of AKT protein expression in both cell lines concurrent with up-regulated BCL2L11 gene. Our results point to the AKT/PI3K signaling pathway as one of the key mechanisms behind SANG-induced cell cycle arrest and death. Conclusion: SANG shows anticancer properties and apoptosis-related gene expression changes in the two TNBC cell lines and suggests AKT/PI3K pathway implication in apoptosis induction and cell cycle arrest. Thus, we propose SANG's potential as a solitary or supplementary treatment agent against TNBC. In the United States, breast cancer (BC) is the most common malignancy and the second leading cause of death among women aged 20-59 years (1). Gene expression is controlled by molecular signal transduction, and alterations in transcriptional settings distinguish cancer cells (2). BC is a heterogeneous cancer type categorized based on its molecular features. Triple-negative breast cancer (TNBC) affects approximately 15% of patients with BC (2). However, the incidence of this subtype is two to three folds higher in African American (AA) women than in other ethnic groups (3, 4). TNBC is the most aggressive BC and has a poor outcome compared to different BC subtypes (3, 5). Based on immunohistochemical characteristics, the expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) are missing in TNBC cells (3, 6). Currently, chemotherapy is the principal treatment for patients with TNBC. However, disease recurrence can manifest within the first two years 323</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="015425d7b9c904c13ed7c50f81785b85" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081022,"asset_id":124950491,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081022/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950491"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950491"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950491; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950491]").text(description); $(".js-view-count[data-work-id=124950491]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950491; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950491']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "015425d7b9c904c13ed7c50f81785b85" } } $('.js-work-strip[data-work-id=124950491]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950491,"title":"Involvement of AKT/PI3K Pathway in Sanguinarine’s Induced Apoptosis and Cell Cycle Arrest in Triple-negative Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Anticancer Research USA Inc.","grobid_abstract":"Background/Aim: Chemotherapy resistance in triple-negative breast cancer (TNBC) cells is well documented. 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Results: SANG lowered cell viability and disrupted cell cycle progression in both cell lines. Furthermore, S-phase cell cycle arrest-mediated apoptosis was found to be the primary contributor to cell growth inhibition in MDA-MB-231 cells. SANG-treated TNBC cells showed significantly up-regulated mRNA expression of 18 genes associated with apoptosis, including eight TNF receptor superfamily (TNFRSF), three members of the BCL2 family, and two members of the caspase (CASP) family in MDA-MB-468 cells. In MDA-MB-231 cells, two members of the TNF superfamily and four members of the BCL2 family were affected. The western study data showed the inhibition of AKT protein expression in both cell lines concurrent with up-regulated BCL2L11 gene. Our results point to the AKT/PI3K signaling pathway as one of the key mechanisms behind SANG-induced cell cycle arrest and death. Conclusion: SANG shows anticancer properties and apoptosis-related gene expression changes in the two TNBC cell lines and suggests AKT/PI3K pathway implication in apoptosis induction and cell cycle arrest. Thus, we propose SANG's potential as a solitary or supplementary treatment agent against TNBC. In the United States, breast cancer (BC) is the most common malignancy and the second leading cause of death among women aged 20-59 years (1). Gene expression is controlled by molecular signal transduction, and alterations in transcriptional settings distinguish cancer cells (2). BC is a heterogeneous cancer type categorized based on its molecular features. Triple-negative breast cancer (TNBC) affects approximately 15% of patients with BC (2). However, the incidence of this subtype is two to three folds higher in African American (AA) women than in other ethnic groups (3, 4). TNBC is the most aggressive BC and has a poor outcome compared to different BC subtypes (3, 5). 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Results: SANG lowered cell viability and disrupted cell cycle progression in both cell lines. Furthermore, S-phase cell cycle arrest-mediated apoptosis was found to be the primary contributor to cell growth inhibition in MDA-MB-231 cells. SANG-treated TNBC cells showed significantly up-regulated mRNA expression of 18 genes associated with apoptosis, including eight TNF receptor superfamily (TNFRSF), three members of the BCL2 family, and two members of the caspase (CASP) family in MDA-MB-468 cells. In MDA-MB-231 cells, two members of the TNF superfamily and four members of the BCL2 family were affected. The western study data showed the inhibition of AKT protein expression in both cell lines concurrent with up-regulated BCL2L11 gene. Our results point to the AKT/PI3K signaling pathway as one of the key mechanisms behind SANG-induced cell cycle arrest and death. Conclusion: SANG shows anticancer properties and apoptosis-related gene expression changes in the two TNBC cell lines and suggests AKT/PI3K pathway implication in apoptosis induction and cell cycle arrest. Thus, we propose SANG's potential as a solitary or supplementary treatment agent against TNBC. In the United States, breast cancer (BC) is the most common malignancy and the second leading cause of death among women aged 20-59 years (1). Gene expression is controlled by molecular signal transduction, and alterations in transcriptional settings distinguish cancer cells (2). BC is a heterogeneous cancer type categorized based on its molecular features. Triple-negative breast cancer (TNBC) affects approximately 15% of patients with BC (2). However, the incidence of this subtype is two to three folds higher in African American (AA) women than in other ethnic groups (3, 4). TNBC is the most aggressive BC and has a poor outcome compared to different BC subtypes (3, 5). Based on immunohistochemical characteristics, the expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) are missing in TNBC cells (3, 6). Currently, chemotherapy is the principal treatment for patients with TNBC. However, disease recurrence can manifest within the first two years 323","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081022,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081022/thumbnails/1.jpg","file_name":"323.full.pdf","download_url":"https://www.academia.edu/attachments/119081022/download_file","bulk_download_file_name":"Involvement_of_AKT_PI3K_Pathway_in_Sangu.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081022/323.full-libre.pdf?1729611369=\u0026response-content-disposition=attachment%3B+filename%3DInvolvement_of_AKT_PI3K_Pathway_in_Sangu.pdf\u0026Expires=1742120023\u0026Signature=UoFUNoYPwnqxTHHDNhUxSxYe1FPKiZdMqMdWYEFyiH6P4bo8Ok-we9khg~AaZBy18QZyWNe0kkut9z4XWno0k3vN3hXukNImw1-QfXeIE2li5MdjdU6dHMU-ws2OdPzqyANoLBOTaDYh3b1FnS-kJpx1SnLSXsxqAwF0~l9nuOHMvDYTkKJ0YSrB9wVfRveMYfKKv7S41LbJ0X8C8hXAQwMbMf9lwExQqZhxq6bsBTIH~UGhMqOX4rFq2Aj1q4~RuINjLV7NHcksTYmFJokpTC9TgJA8p90Gm0YHIQEkgjQlzv36GnecY4FpsqTcYa7~BdY0pJ9LrxSqh0dKNx3e0Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":1290,"name":"Immunology","url":"https://www.academia.edu/Documents/in/Immunology"},{"id":9113,"name":"Cell Cycle","url":"https://www.academia.edu/Documents/in/Cell_Cycle"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"},{"id":1335152,"name":"Viability assay","url":"https://www.academia.edu/Documents/in/Viability_assay"}],"urls":[{"id":45280627,"url":"https://syndication.highwire.org/content/doi/10.21873/cgp.20385"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950490"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950490/Disparities_in_Infant_Nutrition_WIC_Participation_and_Rates_of_Breastfeeding_in_Florida"><img alt="Research paper thumbnail of Disparities in Infant Nutrition: WIC Participation and Rates of Breastfeeding in Florida" class="work-thumbnail" src="https://attachments.academia-assets.com/119080991/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950490/Disparities_in_Infant_Nutrition_WIC_Participation_and_Rates_of_Breastfeeding_in_Florida">Disparities in Infant Nutrition: WIC Participation and Rates of Breastfeeding in Florida</a></div><div class="wp-workCard_item"><span>International Journal of Environmental Research and Public Health</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Being cognizant of the pronounced health advantages of breastfeeding for both the nursing mother ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Being cognizant of the pronounced health advantages of breastfeeding for both the nursing mother and her infant, the breastfeeding dyad, we examined breastfeeding rates among Floridian women who gave birth from 2012 to 2014 (N = 639,052). We investigated the associations between breastfeeding initiation and WIC-based breastfeeding support (the Special Supplemental Nutrition Program for Women, Infants, and Children), education level, and race and ethnicity. We compared the percentage of breastfeeding mothers between those in the WIC program to those who were not, and we compared breastfeeding rates across racial and ethnic groups. Consistent with previous reports, black newborns in this study were breastfed at lower rates than other racial groups, and WIC program participants were less likely to breastfeed than non-WIC program participants. However, by breaking down the data by education level and race, and ethnicity, we see a significantly increased rate of breastfeeding due to WIC ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3a7c71c36da326db6a36429d3e2f4bcd" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119080991,"asset_id":124950490,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119080991/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950490"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950490"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950490; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950490]").text(description); $(".js-view-count[data-work-id=124950490]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950490; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950490']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "3a7c71c36da326db6a36429d3e2f4bcd" } } $('.js-work-strip[data-work-id=124950490]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950490,"title":"Disparities in Infant Nutrition: WIC Participation and Rates of Breastfeeding in Florida","translated_title":"","metadata":{"abstract":"Being cognizant of the pronounced health advantages of breastfeeding for both the nursing mother and her infant, the breastfeeding dyad, we examined breastfeeding rates among Floridian women who gave birth from 2012 to 2014 (N = 639,052). 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950489"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950489/Attenuative_Effect_of_Diallyl_Trisulfide_on_Caspase_Activity_in_TNF_%CE%B1_induced_Triple_Negative_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Attenuative Effect of Diallyl Trisulfide on Caspase Activity in TNF-α-induced Triple Negative Breast Cancer Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081020/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950489/Attenuative_Effect_of_Diallyl_Trisulfide_on_Caspase_Activity_in_TNF_%CE%B1_induced_Triple_Negative_Breast_Cancer_Cells">Attenuative Effect of Diallyl Trisulfide on Caspase Activity in TNF-α-induced Triple Negative Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>Anticancer Research</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit carcinogenesis in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit carcinogenesis in cancer cells. We have previously shown DATS's ability to decrease the percentage of viable cells, inhibit cell migration and modulate genes involved in the nuclear factor kappa-light-chainenhancer of activated B cells (NF-ĸB) and mitogen-activated protein kinase (MAPK) signaling. Materials and Methods: This study aimed to compare the efficacy of DATS in tumor necrosis factor alpha (TNF-α) induced MDA-MB-231 and MDA-MB-468 cells and investigate its role in cell-death signaling via cell cycle, flow cytometry, and caspase assay. Results: DATS exhibit a time-dependent accumulation of G 2 /M phase cells in both cell lines, with higher effects in the MDA-MB-468 for all time points. DATS's ability to decrease the percentage of viable cells in both MDA-MB-231 and MDA-MB-468 cells was shown by a significant but slight increase of early and late apoptosis in the presence of DATS compared to control. Moreover, MDA-MB-468 cells showed more sensitivity to the DATS effect, evidenced by the higher percentage of apoptosis than MDA-MB-231 cells. The caspase studies showed a significant increase in caspase 3 and 8 activity in the presence of DATS, compared to control, in both cell lines. DATS showed no significant increase in caspase 9 activity in both cell lines compared to the control. Conclusion: DATS-induced apoptosis in human breast cancer cells is mediated, at least in part, by cell cycle arrest and caspase activity. These findings provide information for future studies into the role of DATS in TNBC therapy and prevention.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="988ce306719a9cedfcc984b33df7c396" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081020,"asset_id":124950489,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081020/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950489"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950489"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950489; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950489]").text(description); $(".js-view-count[data-work-id=124950489]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950489; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950489']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "988ce306719a9cedfcc984b33df7c396" } } $('.js-work-strip[data-work-id=124950489]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950489,"title":"Attenuative Effect of Diallyl Trisulfide on Caspase Activity in TNF-α-induced Triple Negative Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Anticancer Research USA Inc.","ai_title_tag":"Diallyl Trisulfide Induces Apoptosis in TNF-α TNBC Cells","grobid_abstract":"Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit carcinogenesis in cancer cells. We have previously shown DATS's ability to decrease the percentage of viable cells, inhibit cell migration and modulate genes involved in the nuclear factor kappa-light-chainenhancer of activated B cells (NF-ĸB) and mitogen-activated protein kinase (MAPK) signaling. Materials and Methods: This study aimed to compare the efficacy of DATS in tumor necrosis factor alpha (TNF-α) induced MDA-MB-231 and MDA-MB-468 cells and investigate its role in cell-death signaling via cell cycle, flow cytometry, and caspase assay. Results: DATS exhibit a time-dependent accumulation of G 2 /M phase cells in both cell lines, with higher effects in the MDA-MB-468 for all time points. DATS's ability to decrease the percentage of viable cells in both MDA-MB-231 and MDA-MB-468 cells was shown by a significant but slight increase of early and late apoptosis in the presence of DATS compared to control. Moreover, MDA-MB-468 cells showed more sensitivity to the DATS effect, evidenced by the higher percentage of apoptosis than MDA-MB-231 cells. The caspase studies showed a significant increase in caspase 3 and 8 activity in the presence of DATS, compared to control, in both cell lines. DATS showed no significant increase in caspase 9 activity in both cell lines compared to the control. Conclusion: DATS-induced apoptosis in human breast cancer cells is mediated, at least in part, by cell cycle arrest and caspase activity. These findings provide information for future studies into the role of DATS in TNBC therapy and prevention.","publication_name":"Anticancer Research","grobid_abstract_attachment_id":119081020},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950489/Attenuative_Effect_of_Diallyl_Trisulfide_on_Caspase_Activity_in_TNF_%CE%B1_induced_Triple_Negative_Breast_Cancer_Cells","translated_internal_url":"","created_at":"2024-10-22T08:29:19.669-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081020,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081020/thumbnails/1.jpg","file_name":"2393.full.pdf","download_url":"https://www.academia.edu/attachments/119081020/download_file","bulk_download_file_name":"Attenuative_Effect_of_Diallyl_Trisulfide.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081020/2393.full-libre.pdf?1729611344=\u0026response-content-disposition=attachment%3B+filename%3DAttenuative_Effect_of_Diallyl_Trisulfide.pdf\u0026Expires=1742120023\u0026Signature=L2KAuCxb8ko7XWmyWxqHph7dIktaWkbl714ntLnrOAiLmDWDzcbxOeXHrQDJZA8Qwh3ocDiGJmTWGHBcRLZgL9nVBCXHAnbTqVJlcdSaVrNZf274RrWUchxKdQlU6MjyW0fiVb~sOC32LYkHyk9ns4H4tGPfb-2GqUSYOymva0gYc8F1srTopmwWXShl52KU~BFGf~RUT8BMChac1s925VuG8cKTR9l4JjGC95DbeRoVXjP2Q9jIoZUqAmGLoUMh0YB3MCtctASNPff1RKH51H3cC9FG5WPm3~EwgD10ENZHXCsfGl6nfAl~tmt3CqjXQH9frN5sriqQGhJbTn6WyA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Attenuative_Effect_of_Diallyl_Trisulfide_on_Caspase_Activity_in_TNF_α_induced_Triple_Negative_Breast_Cancer_Cells","translated_slug":"","page_count":13,"language":"en","content_type":"Work","summary":"Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit carcinogenesis in cancer cells. We have previously shown DATS's ability to decrease the percentage of viable cells, inhibit cell migration and modulate genes involved in the nuclear factor kappa-light-chainenhancer of activated B cells (NF-ĸB) and mitogen-activated protein kinase (MAPK) signaling. Materials and Methods: This study aimed to compare the efficacy of DATS in tumor necrosis factor alpha (TNF-α) induced MDA-MB-231 and MDA-MB-468 cells and investigate its role in cell-death signaling via cell cycle, flow cytometry, and caspase assay. Results: DATS exhibit a time-dependent accumulation of G 2 /M phase cells in both cell lines, with higher effects in the MDA-MB-468 for all time points. DATS's ability to decrease the percentage of viable cells in both MDA-MB-231 and MDA-MB-468 cells was shown by a significant but slight increase of early and late apoptosis in the presence of DATS compared to control. Moreover, MDA-MB-468 cells showed more sensitivity to the DATS effect, evidenced by the higher percentage of apoptosis than MDA-MB-231 cells. The caspase studies showed a significant increase in caspase 3 and 8 activity in the presence of DATS, compared to control, in both cell lines. DATS showed no significant increase in caspase 9 activity in both cell lines compared to the control. Conclusion: DATS-induced apoptosis in human breast cancer cells is mediated, at least in part, by cell cycle arrest and caspase activity. These findings provide information for future studies into the role of DATS in TNBC therapy and prevention.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081020,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081020/thumbnails/1.jpg","file_name":"2393.full.pdf","download_url":"https://www.academia.edu/attachments/119081020/download_file","bulk_download_file_name":"Attenuative_Effect_of_Diallyl_Trisulfide.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081020/2393.full-libre.pdf?1729611344=\u0026response-content-disposition=attachment%3B+filename%3DAttenuative_Effect_of_Diallyl_Trisulfide.pdf\u0026Expires=1742120023\u0026Signature=L2KAuCxb8ko7XWmyWxqHph7dIktaWkbl714ntLnrOAiLmDWDzcbxOeXHrQDJZA8Qwh3ocDiGJmTWGHBcRLZgL9nVBCXHAnbTqVJlcdSaVrNZf274RrWUchxKdQlU6MjyW0fiVb~sOC32LYkHyk9ns4H4tGPfb-2GqUSYOymva0gYc8F1srTopmwWXShl52KU~BFGf~RUT8BMChac1s925VuG8cKTR9l4JjGC95DbeRoVXjP2Q9jIoZUqAmGLoUMh0YB3MCtctASNPff1RKH51H3cC9FG5WPm3~EwgD10ENZHXCsfGl6nfAl~tmt3CqjXQH9frN5sriqQGhJbTn6WyA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":263843,"name":"Anticancer","url":"https://www.academia.edu/Documents/in/Anticancer"}],"urls":[{"id":45280625,"url":"https://syndication.highwire.org/content/doi/10.21873/anticanres.16407"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950488"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950488/Herbal_microbiomes_are_plant_specific_and_rich_in_immune_stimulating_pathogen_associated_molecular_pattern_molecules"><img alt="Research paper thumbnail of Herbal microbiomes are plant-specific and rich in immune-stimulating pathogen-associated molecular pattern molecules" class="work-thumbnail" src="https://attachments.academia-assets.com/119081021/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950488/Herbal_microbiomes_are_plant_specific_and_rich_in_immune_stimulating_pathogen_associated_molecular_pattern_molecules">Herbal microbiomes are plant-specific and rich in immune-stimulating pathogen-associated molecular pattern molecules</a></div><div class="wp-workCard_item"><span>ASPET 2023 Annual Meeting Abstract - Drug Discovery and Development</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ID 14491 Poster Board 296 For thousands of years, humans have been orally consuming herbal botani...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ID 14491 Poster Board 296 For thousands of years, humans have been orally consuming herbal botanical medicines, ascribing the beneficial effects to the plant itself. Oddly, we have not yet realized the impact of ingesting dead/live microorganisms in these plants. The residual dead remains of the herbal microbiome can and do leave a trail of thermal and pH-stable immune-stimulating antigenic epitopes with the capacity to act in the human gut. The current study employs a high throughput screening to elucidate the immune-stimulating properties of over-the-counter (OTC) / point-of-sale (POS) herbs. The findings illustrate the existence of an immune active herbal bioactive microbiome, which is plant specific but independent of the plant itself. In this study, an initial high throughput screening of 2535 phytochemicals and OTC/POS'S botanicals was carried out to elucidate pro-inflammatory effects in RAW 264.7 macrophages, with many as potent as positive controls: lipopolysaccharide (LPS) (E.coli 0111:B4). Microbial pathogen-associated molecular pattern molecules (PAMPS) in bio-active herbs were removed from the plants by spin column application, extracts were retested for a bioactive response, and the pH stability of LPS analyzed using a stomach simulation model. Lastly, we reverse cultured the "residual remains" in 7 OTC/POS herbs which were isolated, colonized, and sequenced using Illumina targeting the V4 region of the 16S rRNA gene and the V1-V3 region of the 18S rRNA gene. The obtained results show that Out of 2535 compounds screened, not a single phytochemical or drug (>500 tested) could mimic LPS, which was only observed for 65 "specific" herbal medicine plants, having high concentrations of PAMPS, dominating in roots and oceanic marine sea kelps /algae's [e.g.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="eb9dd3a2655b3df5aa8ad0279baca5b7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081021,"asset_id":124950488,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081021/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950488"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950488"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950488; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950488]").text(description); $(".js-view-count[data-work-id=124950488]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950488; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950488']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "eb9dd3a2655b3df5aa8ad0279baca5b7" } } $('.js-work-strip[data-work-id=124950488]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950488,"title":"Herbal microbiomes are plant-specific and rich in immune-stimulating pathogen-associated molecular pattern molecules","translated_title":"","metadata":{"publisher":"American Society for Pharmacology and Experimental Therapeutics","grobid_abstract":"ID 14491 Poster Board 296 For thousands of years, humans have been orally consuming herbal botanical medicines, ascribing the beneficial effects to the plant itself. Oddly, we have not yet realized the impact of ingesting dead/live microorganisms in these plants. The residual dead remains of the herbal microbiome can and do leave a trail of thermal and pH-stable immune-stimulating antigenic epitopes with the capacity to act in the human gut. The current study employs a high throughput screening to elucidate the immune-stimulating properties of over-the-counter (OTC) / point-of-sale (POS) herbs. The findings illustrate the existence of an immune active herbal bioactive microbiome, which is plant specific but independent of the plant itself. In this study, an initial high throughput screening of 2535 phytochemicals and OTC/POS'S botanicals was carried out to elucidate pro-inflammatory effects in RAW 264.7 macrophages, with many as potent as positive controls: lipopolysaccharide (LPS) (E.coli 0111:B4). Microbial pathogen-associated molecular pattern molecules (PAMPS) in bio-active herbs were removed from the plants by spin column application, extracts were retested for a bioactive response, and the pH stability of LPS analyzed using a stomach simulation model. Lastly, we reverse cultured the \"residual remains\" in 7 OTC/POS herbs which were isolated, colonized, and sequenced using Illumina targeting the V4 region of the 16S rRNA gene and the V1-V3 region of the 18S rRNA gene. The obtained results show that Out of 2535 compounds screened, not a single phytochemical or drug (\u003e500 tested) could mimic LPS, which was only observed for 65 \"specific\" herbal medicine plants, having high concentrations of PAMPS, dominating in roots and oceanic marine sea kelps /algae's [e.g.","publication_name":"ASPET 2023 Annual Meeting Abstract - Drug Discovery and Development","grobid_abstract_attachment_id":119081021},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950488/Herbal_microbiomes_are_plant_specific_and_rich_in_immune_stimulating_pathogen_associated_molecular_pattern_molecules","translated_internal_url":"","created_at":"2024-10-22T08:29:19.307-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081021,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081021/thumbnails/1.jpg","file_name":"296.full.pdf","download_url":"https://www.academia.edu/attachments/119081021/download_file","bulk_download_file_name":"Herbal_microbiomes_are_plant_specific_an.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081021/296.full-libre.pdf?1729611312=\u0026response-content-disposition=attachment%3B+filename%3DHerbal_microbiomes_are_plant_specific_an.pdf\u0026Expires=1742120023\u0026Signature=AuQmv6f4H7CXy4K4WVSgjV1dlme1i0FfPulsU4QnyrJOAbWmYD~vg3zlslikOLDXehyg7Z8eatYu59pIfpnnBmk2ybvHsG1JAyBFxfg2OPjfa8P8U0Cd9LU8RIVWSa7b7S4UuPEI1tExTiJdYJrkiiw6UIbP2wOhmf4Ch0WtcmujKRI-L7kQ8qYuyPiCxPOWdoC3OXiwyg9-pKjvUzQ8TacsifA70iyYfaV6u0JnUvQFGa016PBx5PRLBJbRlOTGdQAVDJiUN8cwIVSTguyILytcXlOU2nJ7lVrNHz~gvNuVOcdOz53lsO6M59td79La730l3Txv08mpXjctQTZKMA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Herbal_microbiomes_are_plant_specific_and_rich_in_immune_stimulating_pathogen_associated_molecular_pattern_molecules","translated_slug":"","page_count":1,"language":"en","content_type":"Work","summary":"ID 14491 Poster Board 296 For thousands of years, humans have been orally consuming herbal botanical medicines, ascribing the beneficial effects to the plant itself. Oddly, we have not yet realized the impact of ingesting dead/live microorganisms in these plants. The residual dead remains of the herbal microbiome can and do leave a trail of thermal and pH-stable immune-stimulating antigenic epitopes with the capacity to act in the human gut. The current study employs a high throughput screening to elucidate the immune-stimulating properties of over-the-counter (OTC) / point-of-sale (POS) herbs. The findings illustrate the existence of an immune active herbal bioactive microbiome, which is plant specific but independent of the plant itself. In this study, an initial high throughput screening of 2535 phytochemicals and OTC/POS'S botanicals was carried out to elucidate pro-inflammatory effects in RAW 264.7 macrophages, with many as potent as positive controls: lipopolysaccharide (LPS) (E.coli 0111:B4). Microbial pathogen-associated molecular pattern molecules (PAMPS) in bio-active herbs were removed from the plants by spin column application, extracts were retested for a bioactive response, and the pH stability of LPS analyzed using a stomach simulation model. Lastly, we reverse cultured the \"residual remains\" in 7 OTC/POS herbs which were isolated, colonized, and sequenced using Illumina targeting the V4 region of the 16S rRNA gene and the V1-V3 region of the 18S rRNA gene. The obtained results show that Out of 2535 compounds screened, not a single phytochemical or drug (\u003e500 tested) could mimic LPS, which was only observed for 65 \"specific\" herbal medicine plants, having high concentrations of PAMPS, dominating in roots and oceanic marine sea kelps /algae's [e.g.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081021,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081021/thumbnails/1.jpg","file_name":"296.full.pdf","download_url":"https://www.academia.edu/attachments/119081021/download_file","bulk_download_file_name":"Herbal_microbiomes_are_plant_specific_an.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081021/296.full-libre.pdf?1729611312=\u0026response-content-disposition=attachment%3B+filename%3DHerbal_microbiomes_are_plant_specific_an.pdf\u0026Expires=1742120023\u0026Signature=AuQmv6f4H7CXy4K4WVSgjV1dlme1i0FfPulsU4QnyrJOAbWmYD~vg3zlslikOLDXehyg7Z8eatYu59pIfpnnBmk2ybvHsG1JAyBFxfg2OPjfa8P8U0Cd9LU8RIVWSa7b7S4UuPEI1tExTiJdYJrkiiw6UIbP2wOhmf4Ch0WtcmujKRI-L7kQ8qYuyPiCxPOWdoC3OXiwyg9-pKjvUzQ8TacsifA70iyYfaV6u0JnUvQFGa016PBx5PRLBJbRlOTGdQAVDJiUN8cwIVSTguyILytcXlOU2nJ7lVrNHz~gvNuVOcdOz53lsO6M59td79La730l3Txv08mpXjctQTZKMA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":324154,"name":"Immune system","url":"https://www.academia.edu/Documents/in/Immune_system"},{"id":348435,"name":"Microbiome","url":"https://www.academia.edu/Documents/in/Microbiome"}],"urls":[{"id":45280624,"url":"https://syndication.highwire.org/content/doi/10.1124/jpet.122.144910"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950487"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950487/Prognostic_and_Therapeutic_Implications_of_Genes_Associated_with_Apoptosis_and_Protein_Protein_Interactions_in_Triple_Negative_Breast_Cancer"><img alt="Research paper thumbnail of Prognostic and Therapeutic Implications of Genes Associated with Apoptosis and Protein-Protein Interactions in Triple-Negative Breast Cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/119081019/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950487/Prognostic_and_Therapeutic_Implications_of_Genes_Associated_with_Apoptosis_and_Protein_Protein_Interactions_in_Triple_Negative_Breast_Cancer">Prognostic and Therapeutic Implications of Genes Associated with Apoptosis and Protein-Protein Interactions in Triple-Negative Breast Cancer</a></div><div class="wp-workCard_item"><span>ASPET 2023 Annual Meeting Abstract - Cancer Pharmacology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ID 54503 Poster Board 446 Triple-negative breast cancer (TNBC) has historically had fewer treatme...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ID 54503 Poster Board 446 Triple-negative breast cancer (TNBC) has historically had fewer treatment alternatives than other breast cancer types. Therefore, it is critical to explore and pinpoint potential biomarkers that could be utilized in treating TNBC. By doing this, we will significantly enhance a patient's prognosis and quality of life. Apoptosis-controlling genes could be manipulated to increase the death of cancer cells. It is essential to comprehend how the genes involved in the apoptotic pathway interact to identify potential therapeutic targets. Therefore, the current study is aimed to evaluate the gene expression, protein-protein interaction (PPI), and transcription factor interaction of 27 apoptosis-regulated genes in TNBC using integrated bioinformatics methods to assess the gene expression, protein-protein interaction (PPI) and transcription factor interaction. Our findings demonstrated that CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were substantially associated with the overall survival rate (OS) difference of TNBC patients. The results also show that breast tissue gene expressions of BNIP3, TNFRSF10B, MCL1, and CASP4 were downregulated compared to normal breast tissue in UALCAN. At the same time, BIK, AKT1, BAD, FADD, DIABLO, and CASP9 were downregulated in bc-GeneEx-Miner v4.5 mRNA expression (BCGM) databases. Based on the GO term enrichment analysis, the Cellular process (GO:0009987), which has about 21 apoptosis-regulated genes, is the top category in the biological process (BP), followed by biological regulation (GO:0065007). We identified 29 pathways, including p53, angiogenesis, and apoptosis signaling. We examined the PPIs between the genes that regulate apoptosis; CASP3 and CASP9 interact with FADD, MCL1, TNF, TNFRSRF10A, and TNFRSF10; additionally, CASP3 significantly forms PPIs with CASP9, DFFA, and TP53, while CASP9 with DIABLO. In the top 10 transcription factors, the androgen receptor (AR) interacts with five apoptosis-regulated genes (p<0.0001; q<0.01), followed by RARA (Retinoic Acid Receptor Alpha) (p<0.0001; q<0.01) and RNF2 (Ring Finger Protein) (p<0.0001; q<0.01). Overall, the gene expression profile, the PPIs, and the apoptosis-TF interaction findings suggested that the 27 apoptosis-regulated genes might be used as promising targets in treating and managing TNBC. Furthermore, from a total of 27 key genes, CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were significantly correlated with poor overall survival in TNBC (p-value < 0.05), which could play essential roles in the progression of TNBC and provide attractive therapeutic targets that may offer new candidate molecules for targeted therapy. It was concluded from this study that genetic alterations altering apoptosis could be possible biomarkers for the prognosis and facilitate the search for alternative treatment targets for TNBC.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="575df43c5467fd03d435f17615d9ac93" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081019,"asset_id":124950487,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081019/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950487"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950487"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950487; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950487]").text(description); $(".js-view-count[data-work-id=124950487]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950487; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950487']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "575df43c5467fd03d435f17615d9ac93" } } $('.js-work-strip[data-work-id=124950487]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950487,"title":"Prognostic and Therapeutic Implications of Genes Associated with Apoptosis and Protein-Protein Interactions in Triple-Negative Breast Cancer","translated_title":"","metadata":{"publisher":"American Society for Pharmacology and Experimental Therapeutics","grobid_abstract":"ID 54503 Poster Board 446 Triple-negative breast cancer (TNBC) has historically had fewer treatment alternatives than other breast cancer types. Therefore, it is critical to explore and pinpoint potential biomarkers that could be utilized in treating TNBC. By doing this, we will significantly enhance a patient's prognosis and quality of life. Apoptosis-controlling genes could be manipulated to increase the death of cancer cells. It is essential to comprehend how the genes involved in the apoptotic pathway interact to identify potential therapeutic targets. Therefore, the current study is aimed to evaluate the gene expression, protein-protein interaction (PPI), and transcription factor interaction of 27 apoptosis-regulated genes in TNBC using integrated bioinformatics methods to assess the gene expression, protein-protein interaction (PPI) and transcription factor interaction. Our findings demonstrated that CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were substantially associated with the overall survival rate (OS) difference of TNBC patients. The results also show that breast tissue gene expressions of BNIP3, TNFRSF10B, MCL1, and CASP4 were downregulated compared to normal breast tissue in UALCAN. At the same time, BIK, AKT1, BAD, FADD, DIABLO, and CASP9 were downregulated in bc-GeneEx-Miner v4.5 mRNA expression (BCGM) databases. Based on the GO term enrichment analysis, the Cellular process (GO:0009987), which has about 21 apoptosis-regulated genes, is the top category in the biological process (BP), followed by biological regulation (GO:0065007). We identified 29 pathways, including p53, angiogenesis, and apoptosis signaling. We examined the PPIs between the genes that regulate apoptosis; CASP3 and CASP9 interact with FADD, MCL1, TNF, TNFRSRF10A, and TNFRSF10; additionally, CASP3 significantly forms PPIs with CASP9, DFFA, and TP53, while CASP9 with DIABLO. In the top 10 transcription factors, the androgen receptor (AR) interacts with five apoptosis-regulated genes (p\u003c0.0001; q\u003c0.01), followed by RARA (Retinoic Acid Receptor Alpha) (p\u003c0.0001; q\u003c0.01) and RNF2 (Ring Finger Protein) (p\u003c0.0001; q\u003c0.01). Overall, the gene expression profile, the PPIs, and the apoptosis-TF interaction findings suggested that the 27 apoptosis-regulated genes might be used as promising targets in treating and managing TNBC. Furthermore, from a total of 27 key genes, CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were significantly correlated with poor overall survival in TNBC (p-value \u003c 0.05), which could play essential roles in the progression of TNBC and provide attractive therapeutic targets that may offer new candidate molecules for targeted therapy. 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Therefore, it is critical to explore and pinpoint potential biomarkers that could be utilized in treating TNBC. By doing this, we will significantly enhance a patient's prognosis and quality of life. Apoptosis-controlling genes could be manipulated to increase the death of cancer cells. It is essential to comprehend how the genes involved in the apoptotic pathway interact to identify potential therapeutic targets. Therefore, the current study is aimed to evaluate the gene expression, protein-protein interaction (PPI), and transcription factor interaction of 27 apoptosis-regulated genes in TNBC using integrated bioinformatics methods to assess the gene expression, protein-protein interaction (PPI) and transcription factor interaction. Our findings demonstrated that CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were substantially associated with the overall survival rate (OS) difference of TNBC patients. The results also show that breast tissue gene expressions of BNIP3, TNFRSF10B, MCL1, and CASP4 were downregulated compared to normal breast tissue in UALCAN. At the same time, BIK, AKT1, BAD, FADD, DIABLO, and CASP9 were downregulated in bc-GeneEx-Miner v4.5 mRNA expression (BCGM) databases. Based on the GO term enrichment analysis, the Cellular process (GO:0009987), which has about 21 apoptosis-regulated genes, is the top category in the biological process (BP), followed by biological regulation (GO:0065007). We identified 29 pathways, including p53, angiogenesis, and apoptosis signaling. We examined the PPIs between the genes that regulate apoptosis; CASP3 and CASP9 interact with FADD, MCL1, TNF, TNFRSRF10A, and TNFRSF10; additionally, CASP3 significantly forms PPIs with CASP9, DFFA, and TP53, while CASP9 with DIABLO. In the top 10 transcription factors, the androgen receptor (AR) interacts with five apoptosis-regulated genes (p\u003c0.0001; q\u003c0.01), followed by RARA (Retinoic Acid Receptor Alpha) (p\u003c0.0001; q\u003c0.01) and RNF2 (Ring Finger Protein) (p\u003c0.0001; q\u003c0.01). Overall, the gene expression profile, the PPIs, and the apoptosis-TF interaction findings suggested that the 27 apoptosis-regulated genes might be used as promising targets in treating and managing TNBC. Furthermore, from a total of 27 key genes, CASP2, CASP3, DAPK1, TNF, TRAF2, and TRAF3 were significantly correlated with poor overall survival in TNBC (p-value \u003c 0.05), which could play essential roles in the progression of TNBC and provide attractive therapeutic targets that may offer new candidate molecules for targeted therapy. It was concluded from this study that genetic alterations altering apoptosis could be possible biomarkers for the prognosis and facilitate the search for alternative treatment targets for TNBC.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081019,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081019/thumbnails/1.jpg","file_name":"446.full.pdf","download_url":"https://www.academia.edu/attachments/119081019/download_file","bulk_download_file_name":"Prognostic_and_Therapeutic_Implications.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081019/446.full-libre.pdf?1729611315=\u0026response-content-disposition=attachment%3B+filename%3DPrognostic_and_Therapeutic_Implications.pdf\u0026Expires=1742120023\u0026Signature=Fg2o4XElxETn3I~etDfPU67iwKaL1anjjl9uJEJ4LR8g-6KesvHNAlvYm7InnHfUxP-dQpS1yjvLPPldLTL~ajFhzVhD06CLga2VffzRzwwtN0omNAfeMGICcwF0UdCZn-hM1dUakvfb6ZPMHocNUBCTHG3ZmV3ulySp744SrnMcPKMeMHftKYm7SIkivRNa~wziSm~ML3E4SUr8UWhwyDHeBZ1ZhtCG1zwYx~gszLSJstUbNOKCWVPUe0-SuAa6w-TAaazv8SYlLrVvoPwKCniZn6FHxv~VAP6ci0oiZc3J-WYSg0XHEb1VSWO~YhuaxTr6NgpdCP1kQuUs6pPkwQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":6802,"name":"Breast Cancer","url":"https://www.academia.edu/Documents/in/Breast_Cancer"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":181936,"name":"Gene","url":"https://www.academia.edu/Documents/in/Gene"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"}],"urls":[{"id":45280623,"url":"https://syndication.highwire.org/content/doi/10.1124/jpet.122.545030"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950486"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950486/Transcriptome_Profiling_During_Muscadine_Berry_Development_Reveals_the_Dynamic_of_Polyphenols_Metabolism"><img alt="Research paper thumbnail of Transcriptome Profiling During Muscadine Berry Development Reveals the Dynamic of Polyphenols Metabolism" class="work-thumbnail" src="https://attachments.academia-assets.com/119081016/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950486/Transcriptome_Profiling_During_Muscadine_Berry_Development_Reveals_the_Dynamic_of_Polyphenols_Metabolism">Transcriptome Profiling During Muscadine Berry Development Reveals the Dynamic of Polyphenols Metabolism</a></div><div class="wp-workCard_item"><span>Frontiers in Plant Science</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape speci...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape species. To identify the molecular events associated with polyphenolic accumulation that influence antioxidant capacity, two contrasting muscadine genotypes (C5 and C6) with varied phenolic/flavonoid content and antioxidant activity were investigatedviaRNA-sequencing during berry development. The results showed that berry development is concomitant with transcriptome profile changes, which was more pronounced at the véraison (V) stage. Despite that the downregulation pattern of gene expression dominated the upregulation through berry development, the C5 genotype maintained higher expression levels. Comparative transcript profiling allowed the identification of 94 differentially expressed genes with potential relevance in regulating fruit secondary metabolism, including 18 transcription factors and 76 structural genes. The genes underlying the critical enzymes in the modification reactions of ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="6c1adeb698213f60edf3e33711043a45" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081016,"asset_id":124950486,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081016/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950486"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950486"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950486; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950486]").text(description); $(".js-view-count[data-work-id=124950486]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950486; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950486']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "6c1adeb698213f60edf3e33711043a45" } } $('.js-work-strip[data-work-id=124950486]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950486,"title":"Transcriptome Profiling During Muscadine Berry Development Reveals the Dynamic of Polyphenols Metabolism","translated_title":"","metadata":{"abstract":"Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape species. To identify the molecular events associated with polyphenolic accumulation that influence antioxidant capacity, two contrasting muscadine genotypes (C5 and C6) with varied phenolic/flavonoid content and antioxidant activity were investigatedviaRNA-sequencing during berry development. The results showed that berry development is concomitant with transcriptome profile changes, which was more pronounced at the véraison (V) stage. Despite that the downregulation pattern of gene expression dominated the upregulation through berry development, the C5 genotype maintained higher expression levels. Comparative transcript profiling allowed the identification of 94 differentially expressed genes with potential relevance in regulating fruit secondary metabolism, including 18 transcription factors and 76 structural genes. The genes underlying the critical enzymes in the modification reactions of ...","publisher":"Frontiers Media SA","publication_name":"Frontiers in Plant Science"},"translated_abstract":"Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape species. To identify the molecular events associated with polyphenolic accumulation that influence antioxidant capacity, two contrasting muscadine genotypes (C5 and C6) with varied phenolic/flavonoid content and antioxidant activity were investigatedviaRNA-sequencing during berry development. The results showed that berry development is concomitant with transcriptome profile changes, which was more pronounced at the véraison (V) stage. Despite that the downregulation pattern of gene expression dominated the upregulation through berry development, the C5 genotype maintained higher expression levels. Comparative transcript profiling allowed the identification of 94 differentially expressed genes with potential relevance in regulating fruit secondary metabolism, including 18 transcription factors and 76 structural genes. The genes underlying the critical enzymes in the modification reactions of ...","internal_url":"https://www.academia.edu/124950486/Transcriptome_Profiling_During_Muscadine_Berry_Development_Reveals_the_Dynamic_of_Polyphenols_Metabolism","translated_internal_url":"","created_at":"2024-10-22T08:29:18.750-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081016,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081016/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081016/download_file","bulk_download_file_name":"Transcriptome_Profiling_During_Muscadine.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081016/pdf-libre.pdf?1729611330=\u0026response-content-disposition=attachment%3B+filename%3DTranscriptome_Profiling_During_Muscadine.pdf\u0026Expires=1742120023\u0026Signature=PXAezDil4kGIZ2H-3zgmcWvrW2VJ-r-wIM3qPLcVFRGTfscu2VAQuOTv7Uvhq5RD2FAcrBAi-J0D6x8mTH1K1nFi4oExgaHdeAYg00nyT7gq~pM47-UJNHyONMnqgKSKiVyADlzs9jfCX6tek~TSQhrXUy~6KBuy15mbWGIC51sfkTAkMg3~kCNne9-xz0e~OZto0ALcyebstB-4U0jNlBIbtmMbylmnLWJThE0qS2uo7L6lTo87E06xSmoBB92-4QVzpR-tEpHaPTKET0ijBosZil2gv0kcyRd92Fk5MLao3YI8M-9RD1S5bvHHqc00qRK3e4b2HFYCRgFMvWaNsA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Transcriptome_Profiling_During_Muscadine_Berry_Development_Reveals_the_Dynamic_of_Polyphenols_Metabolism","translated_slug":"","page_count":17,"language":"en","content_type":"Work","summary":"Muscadine grapes accumulate higher amounts of bioactive phenolics compared with other grape species. To identify the molecular events associated with polyphenolic accumulation that influence antioxidant capacity, two contrasting muscadine genotypes (C5 and C6) with varied phenolic/flavonoid content and antioxidant activity were investigatedviaRNA-sequencing during berry development. The results showed that berry development is concomitant with transcriptome profile changes, which was more pronounced at the véraison (V) stage. Despite that the downregulation pattern of gene expression dominated the upregulation through berry development, the C5 genotype maintained higher expression levels. Comparative transcript profiling allowed the identification of 94 differentially expressed genes with potential relevance in regulating fruit secondary metabolism, including 18 transcription factors and 76 structural genes. The genes underlying the critical enzymes in the modification reactions of ...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081016,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081016/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081016/download_file","bulk_download_file_name":"Transcriptome_Profiling_During_Muscadine.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081016/pdf-libre.pdf?1729611330=\u0026response-content-disposition=attachment%3B+filename%3DTranscriptome_Profiling_During_Muscadine.pdf\u0026Expires=1742120023\u0026Signature=PXAezDil4kGIZ2H-3zgmcWvrW2VJ-r-wIM3qPLcVFRGTfscu2VAQuOTv7Uvhq5RD2FAcrBAi-J0D6x8mTH1K1nFi4oExgaHdeAYg00nyT7gq~pM47-UJNHyONMnqgKSKiVyADlzs9jfCX6tek~TSQhrXUy~6KBuy15mbWGIC51sfkTAkMg3~kCNne9-xz0e~OZto0ALcyebstB-4U0jNlBIbtmMbylmnLWJThE0qS2uo7L6lTo87E06xSmoBB92-4QVzpR-tEpHaPTKET0ijBosZil2gv0kcyRd92Fk5MLao3YI8M-9RD1S5bvHHqc00qRK3e4b2HFYCRgFMvWaNsA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":43761,"name":"Transcriptome","url":"https://www.academia.edu/Documents/in/Transcriptome"},{"id":94697,"name":"Plant Secondary Metabolism","url":"https://www.academia.edu/Documents/in/Plant_Secondary_Metabolism"},{"id":732057,"name":"Flavonoid","url":"https://www.academia.edu/Documents/in/Flavonoid"},{"id":832148,"name":"Polyphenol","url":"https://www.academia.edu/Documents/in/Polyphenol"},{"id":980353,"name":"Berry","url":"https://www.academia.edu/Documents/in/Berry"},{"id":1810445,"name":"Gene expression profiling","url":"https://www.academia.edu/Documents/in/Gene_expression_profiling"}],"urls":[{"id":45280622,"url":"https://www.frontiersin.org/articles/10.3389/fpls.2021.818071/full"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950485"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950485/A_multi_locus_genome_wide_association_study_reveals_the_genetics_underlying_muscadine_antioxidant_in_berry_skin"><img alt="Research paper thumbnail of A multi-locus genome-wide association study reveals the genetics underlying muscadine antioxidant in berry skin" class="work-thumbnail" src="https://attachments.academia-assets.com/119081017/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950485/A_multi_locus_genome_wide_association_study_reveals_the_genetics_underlying_muscadine_antioxidant_in_berry_skin">A multi-locus genome-wide association study reveals the genetics underlying muscadine antioxidant in berry skin</a></div><div class="wp-workCard_item"><span>Frontiers in Plant Science</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phy...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phytochemical constituents with great potential antioxidant activity. Such nutritional and health merits are not only restricted to muscadine, but muscadine berries accumulate higher amounts of bioactive polyphenolics compared with other grape species. For the genetic study of the antioxidant trait in muscadine, a multi-locus genome-wide association study (GWAS) with 350 muscadine genotypes and 1,283 RNase H2 enzyme-dependent amplicon sequencing (rhAmpSeq) markers was performed. Phenotyping was conducted with several antioxidant-related traits, including total phenolic content (TPC), total flavonoid content (TFC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity, and FRAP antioxidant assay in muscadine berry skin. The correlation coefficient analysis revealed that the TPC, and DPPH/FRAP activities were significantly correlated. Through the GWAS analysis, 12 QTNs were id...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="35f8ee2e9ef448c0acd58cf64ba4d046" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081017,"asset_id":124950485,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081017/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950485"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950485"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950485; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950485]").text(description); $(".js-view-count[data-work-id=124950485]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950485; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950485']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "35f8ee2e9ef448c0acd58cf64ba4d046" } } $('.js-work-strip[data-work-id=124950485]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950485,"title":"A multi-locus genome-wide association study reveals the genetics underlying muscadine antioxidant in berry skin","translated_title":"","metadata":{"abstract":"Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phytochemical constituents with great potential antioxidant activity. Such nutritional and health merits are not only restricted to muscadine, but muscadine berries accumulate higher amounts of bioactive polyphenolics compared with other grape species. For the genetic study of the antioxidant trait in muscadine, a multi-locus genome-wide association study (GWAS) with 350 muscadine genotypes and 1,283 RNase H2 enzyme-dependent amplicon sequencing (rhAmpSeq) markers was performed. Phenotyping was conducted with several antioxidant-related traits, including total phenolic content (TPC), total flavonoid content (TFC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity, and FRAP antioxidant assay in muscadine berry skin. The correlation coefficient analysis revealed that the TPC, and DPPH/FRAP activities were significantly correlated. Through the GWAS analysis, 12 QTNs were id...","publisher":"Frontiers Media SA","publication_name":"Frontiers in Plant Science"},"translated_abstract":"Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phytochemical constituents with great potential antioxidant activity. Such nutritional and health merits are not only restricted to muscadine, but muscadine berries accumulate higher amounts of bioactive polyphenolics compared with other grape species. For the genetic study of the antioxidant trait in muscadine, a multi-locus genome-wide association study (GWAS) with 350 muscadine genotypes and 1,283 RNase H2 enzyme-dependent amplicon sequencing (rhAmpSeq) markers was performed. Phenotyping was conducted with several antioxidant-related traits, including total phenolic content (TPC), total flavonoid content (TFC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity, and FRAP antioxidant assay in muscadine berry skin. The correlation coefficient analysis revealed that the TPC, and DPPH/FRAP activities were significantly correlated. Through the GWAS analysis, 12 QTNs were id...","internal_url":"https://www.academia.edu/124950485/A_multi_locus_genome_wide_association_study_reveals_the_genetics_underlying_muscadine_antioxidant_in_berry_skin","translated_internal_url":"","created_at":"2024-10-22T08:29:18.483-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081017,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081017/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081017/download_file","bulk_download_file_name":"A_multi_locus_genome_wide_association_st.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081017/pdf-libre.pdf?1729611330=\u0026response-content-disposition=attachment%3B+filename%3DA_multi_locus_genome_wide_association_st.pdf\u0026Expires=1742120023\u0026Signature=IL-IOHijvakpYD0x8HQHqJI897oxKZzn5mqg0Am0ezoJgSGq29ydv1r~Ikajrnzliu~yduoxBTPq7fYKRmz3UoGrm8ZWV2lU1Y8mh79-dAegR6jb62ynIFTzsUvFzoPXLbT7izcx2n1Jo45gG2oqc-t2c~IfLKyr9GxkkZgTwkk0PE7QFew1e8sjWfTxc-sxTNIHL30y3tM6193JkrOQ2j5hi22A2SIZAN4gOM6rdxVDjNkJaQ3t7VkcFxw7UMke~xpd4aHymYpuc7oWCSuzJLfpv9lBRRYT0R3gNGSWUvXnc6SwzsRF0DsKV0OSz85JWkGtLbw4GQFik6DwA4v12w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"A_multi_locus_genome_wide_association_study_reveals_the_genetics_underlying_muscadine_antioxidant_in_berry_skin","translated_slug":"","page_count":12,"language":"en","content_type":"Work","summary":"Muscadine berries display enhanced nutraceutical value due to the accumulation of distinctive phytochemical constituents with great potential antioxidant activity. Such nutritional and health merits are not only restricted to muscadine, but muscadine berries accumulate higher amounts of bioactive polyphenolics compared with other grape species. For the genetic study of the antioxidant trait in muscadine, a multi-locus genome-wide association study (GWAS) with 350 muscadine genotypes and 1,283 RNase H2 enzyme-dependent amplicon sequencing (rhAmpSeq) markers was performed. Phenotyping was conducted with several antioxidant-related traits, including total phenolic content (TPC), total flavonoid content (TFC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity, and FRAP antioxidant assay in muscadine berry skin. The correlation coefficient analysis revealed that the TPC, and DPPH/FRAP activities were significantly correlated. Through the GWAS analysis, 12 QTNs were id...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081017,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081017/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081017/download_file","bulk_download_file_name":"A_multi_locus_genome_wide_association_st.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081017/pdf-libre.pdf?1729611330=\u0026response-content-disposition=attachment%3B+filename%3DA_multi_locus_genome_wide_association_st.pdf\u0026Expires=1742120023\u0026Signature=IL-IOHijvakpYD0x8HQHqJI897oxKZzn5mqg0Am0ezoJgSGq29ydv1r~Ikajrnzliu~yduoxBTPq7fYKRmz3UoGrm8ZWV2lU1Y8mh79-dAegR6jb62ynIFTzsUvFzoPXLbT7izcx2n1Jo45gG2oqc-t2c~IfLKyr9GxkkZgTwkk0PE7QFew1e8sjWfTxc-sxTNIHL30y3tM6193JkrOQ2j5hi22A2SIZAN4gOM6rdxVDjNkJaQ3t7VkcFxw7UMke~xpd4aHymYpuc7oWCSuzJLfpv9lBRRYT0R3gNGSWUvXnc6SwzsRF0DsKV0OSz85JWkGtLbw4GQFik6DwA4v12w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":382472,"name":"DPPH","url":"https://www.academia.edu/Documents/in/DPPH"}],"urls":[{"id":45280621,"url":"https://www.frontiersin.org/articles/10.3389/fpls.2022.969301/full"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950484"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950484/Abstract_PO_116_Pentagalloyl_glucose_inhibits_GRO_%CE%B1_CXCL1_pro_inflammatory_cytokine_and_induces_expression_of_apoptosis_related_genes_in_racially_different_TNBC_cells"><img alt="Research paper thumbnail of Abstract PO-116: Pentagalloyl glucose inhibits GRO-α/CXCL1 pro-inflammatory cytokine and induces expression of apoptosis-related genes in racially different TNBC cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950484/Abstract_PO_116_Pentagalloyl_glucose_inhibits_GRO_%CE%B1_CXCL1_pro_inflammatory_cytokine_and_induces_expression_of_apoptosis_related_genes_in_racially_different_TNBC_cells">Abstract PO-116: Pentagalloyl glucose inhibits GRO-α/CXCL1 pro-inflammatory cytokine and induces expression of apoptosis-related genes in racially different TNBC cells</a></div><div class="wp-workCard_item"><span>Cancer Epidemiology, Biomarkers &amp; Prevention</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A distinctive tumor microenvironment associated with chronic inflammation, cancer development, an...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A distinctive tumor microenvironment associated with chronic inflammation, cancer development, and drug resistance in triple-negative breast cancer (TNBC) affect disproportionally Caucasian and African American women. PURPOSE: This investigation presents possible new biomarkers that could be modulated by the natural compound pentagalloyl glucose (PGG) in MM-231 (Caucasians) and MM-468 (African American) TNBC cells. METHODS: Cytokine arrays, ELISA, RT-PCR, flow cytometry, and Western analysis were performed. RESULTS: PGG reduced the expression of GRO-α/CXCL1 pro-inflammatory cytokine, which is associated with tumor recurrence and chemoresistance. PGG inhibited IκBKE and MAPK1 gene and protein expression indicating a possible signaling pathway for CXCL1 downregulation through NFκB and MAPK signaling. PGG also inhibited cell growth in both cell lines, which could be associated with a decrease in CXCL1 levels. Besides, PGG induced apoptosis, modulating numerous genes, including caspases...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950484"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950484"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950484; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950484]").text(description); $(".js-view-count[data-work-id=124950484]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950484; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950484']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950484]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950484,"title":"Abstract PO-116: Pentagalloyl glucose inhibits GRO-α/CXCL1 pro-inflammatory cytokine and induces expression of apoptosis-related genes in racially different TNBC cells","translated_title":"","metadata":{"abstract":"A distinctive tumor microenvironment associated with chronic inflammation, cancer development, and drug resistance in triple-negative breast cancer (TNBC) affect disproportionally Caucasian and African American women. PURPOSE: This investigation presents possible new biomarkers that could be modulated by the natural compound pentagalloyl glucose (PGG) in MM-231 (Caucasians) and MM-468 (African American) TNBC cells. METHODS: Cytokine arrays, ELISA, RT-PCR, flow cytometry, and Western analysis were performed. RESULTS: PGG reduced the expression of GRO-α/CXCL1 pro-inflammatory cytokine, which is associated with tumor recurrence and chemoresistance. PGG inhibited IκBKE and MAPK1 gene and protein expression indicating a possible signaling pathway for CXCL1 downregulation through NFκB and MAPK signaling. PGG also inhibited cell growth in both cell lines, which could be associated with a decrease in CXCL1 levels. Besides, PGG induced apoptosis, modulating numerous genes, including caspases...","publisher":"American Association for Cancer Research (AACR)","publication_name":"Cancer Epidemiology, Biomarkers \u0026amp; Prevention"},"translated_abstract":"A distinctive tumor microenvironment associated with chronic inflammation, cancer development, and drug resistance in triple-negative breast cancer (TNBC) affect disproportionally Caucasian and African American women. PURPOSE: This investigation presents possible new biomarkers that could be modulated by the natural compound pentagalloyl glucose (PGG) in MM-231 (Caucasians) and MM-468 (African American) TNBC cells. METHODS: Cytokine arrays, ELISA, RT-PCR, flow cytometry, and Western analysis were performed. RESULTS: PGG reduced the expression of GRO-α/CXCL1 pro-inflammatory cytokine, which is associated with tumor recurrence and chemoresistance. PGG inhibited IκBKE and MAPK1 gene and protein expression indicating a possible signaling pathway for CXCL1 downregulation through NFκB and MAPK signaling. PGG also inhibited cell growth in both cell lines, which could be associated with a decrease in CXCL1 levels. Besides, PGG induced apoptosis, modulating numerous genes, including caspases...","internal_url":"https://www.academia.edu/124950484/Abstract_PO_116_Pentagalloyl_glucose_inhibits_GRO_%CE%B1_CXCL1_pro_inflammatory_cytokine_and_induces_expression_of_apoptosis_related_genes_in_racially_different_TNBC_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:18.240-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Abstract_PO_116_Pentagalloyl_glucose_inhibits_GRO_α_CXCL1_pro_inflammatory_cytokine_and_induces_expression_of_apoptosis_related_genes_in_racially_different_TNBC_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"A distinctive tumor microenvironment associated with chronic inflammation, cancer development, and drug resistance in triple-negative breast cancer (TNBC) affect disproportionally Caucasian and African American women. PURPOSE: This investigation presents possible new biomarkers that could be modulated by the natural compound pentagalloyl glucose (PGG) in MM-231 (Caucasians) and MM-468 (African American) TNBC cells. METHODS: Cytokine arrays, ELISA, RT-PCR, flow cytometry, and Western analysis were performed. RESULTS: PGG reduced the expression of GRO-α/CXCL1 pro-inflammatory cytokine, which is associated with tumor recurrence and chemoresistance. PGG inhibited IκBKE and MAPK1 gene and protein expression indicating a possible signaling pathway for CXCL1 downregulation through NFκB and MAPK signaling. PGG also inhibited cell growth in both cell lines, which could be associated with a decrease in CXCL1 levels. Besides, PGG induced apoptosis, modulating numerous genes, including caspases...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":295233,"name":"Cytokine","url":"https://www.academia.edu/Documents/in/Cytokine"},{"id":474029,"name":"Tumor necrosis factor-alpha","url":"https://www.academia.edu/Documents/in/Tumor_necrosis_factor-alpha"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":45280620,"url":"https://aacrjournals.org/cebp/article/29/12_Supplement/PO-116/181620/Abstract-PO-116-Pentagalloyl-glucose-inhibits-GRO"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950483"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950483/Abstract_PO_132_Rosmarinic_acid_induced_apoptosis_and_cell_cycle_arrest_in_triple_negative_breast_cancer_cells"><img alt="Research paper thumbnail of Abstract PO-132: Rosmarinic acid-induced apoptosis and cell cycle arrest in triple-negative breast cancer cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950483/Abstract_PO_132_Rosmarinic_acid_induced_apoptosis_and_cell_cycle_arrest_in_triple_negative_breast_cancer_cells">Abstract PO-132: Rosmarinic acid-induced apoptosis and cell cycle arrest in triple-negative breast cancer cells</a></div><div class="wp-workCard_item"><span>Cancer Epidemiology, Biomarkers &amp; Prevention</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, includin...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, including anti-inflammatory, immunomodulatory, anti-mutagenic, antioxidant, and anticancer activities. This study evaluated the effects of RA in two racially different triple-negative breast cancer (TNBC) cell lines. One cell line was derived from Caucasian origin (MDA-MB-231), and another one was derived from an African American origin (MDA-MB-468). The apoptotic effect of RA was performed using An Annexin V-FITC Apoptosis Detection Kit, while the Propidium Iodide Flow Cytometry Kit was used to detect the cell cycle distribution. Gene expression profiling was established using Human Apoptosis PCR array. The results obtained show that RA significantly caused cytotoxic and antiproliferative effects in both cell lines in a dose- and time-dependent manner. It was noted that RA induced cell cycle arrest-related apoptosis and altered the expression of many apoptosis-involved genes differently. In MDA...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950483"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950483"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950483; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950483]").text(description); $(".js-view-count[data-work-id=124950483]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950483; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950483']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950483]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950483,"title":"Abstract PO-132: Rosmarinic acid-induced apoptosis and cell cycle arrest in triple-negative breast cancer cells","translated_title":"","metadata":{"abstract":"Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, including anti-inflammatory, immunomodulatory, anti-mutagenic, antioxidant, and anticancer activities. This study evaluated the effects of RA in two racially different triple-negative breast cancer (TNBC) cell lines. One cell line was derived from Caucasian origin (MDA-MB-231), and another one was derived from an African American origin (MDA-MB-468). The apoptotic effect of RA was performed using An Annexin V-FITC Apoptosis Detection Kit, while the Propidium Iodide Flow Cytometry Kit was used to detect the cell cycle distribution. Gene expression profiling was established using Human Apoptosis PCR array. The results obtained show that RA significantly caused cytotoxic and antiproliferative effects in both cell lines in a dose- and time-dependent manner. It was noted that RA induced cell cycle arrest-related apoptosis and altered the expression of many apoptosis-involved genes differently. In MDA...","publisher":"American Association for Cancer Research (AACR)","publication_name":"Cancer Epidemiology, Biomarkers \u0026amp; Prevention"},"translated_abstract":"Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, including anti-inflammatory, immunomodulatory, anti-mutagenic, antioxidant, and anticancer activities. This study evaluated the effects of RA in two racially different triple-negative breast cancer (TNBC) cell lines. One cell line was derived from Caucasian origin (MDA-MB-231), and another one was derived from an African American origin (MDA-MB-468). The apoptotic effect of RA was performed using An Annexin V-FITC Apoptosis Detection Kit, while the Propidium Iodide Flow Cytometry Kit was used to detect the cell cycle distribution. Gene expression profiling was established using Human Apoptosis PCR array. The results obtained show that RA significantly caused cytotoxic and antiproliferative effects in both cell lines in a dose- and time-dependent manner. It was noted that RA induced cell cycle arrest-related apoptosis and altered the expression of many apoptosis-involved genes differently. In MDA...","internal_url":"https://www.academia.edu/124950483/Abstract_PO_132_Rosmarinic_acid_induced_apoptosis_and_cell_cycle_arrest_in_triple_negative_breast_cancer_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:17.965-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Abstract_PO_132_Rosmarinic_acid_induced_apoptosis_and_cell_cycle_arrest_in_triple_negative_breast_cancer_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Rosmarinic acid (RA) is a polyphenolic compound with various pharmacological properties, including anti-inflammatory, immunomodulatory, anti-mutagenic, antioxidant, and anticancer activities. This study evaluated the effects of RA in two racially different triple-negative breast cancer (TNBC) cell lines. One cell line was derived from Caucasian origin (MDA-MB-231), and another one was derived from an African American origin (MDA-MB-468). The apoptotic effect of RA was performed using An Annexin V-FITC Apoptosis Detection Kit, while the Propidium Iodide Flow Cytometry Kit was used to detect the cell cycle distribution. Gene expression profiling was established using Human Apoptosis PCR array. The results obtained show that RA significantly caused cytotoxic and antiproliferative effects in both cell lines in a dose- and time-dependent manner. It was noted that RA induced cell cycle arrest-related apoptosis and altered the expression of many apoptosis-involved genes differently. In MDA...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":9113,"name":"Cell Cycle","url":"https://www.academia.edu/Documents/in/Cell_Cycle"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":1335154,"name":"Propidium Iodide","url":"https://www.academia.edu/Documents/in/Propidium_Iodide"},{"id":3101476,"name":"Annexin","url":"https://www.academia.edu/Documents/in/Annexin"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":45280619,"url":"https://aacrjournals.org/cebp/article/29/12_Supplement/PO-132/181580/Abstract-PO-132-Rosmarinic-acid-induced-apoptosis"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950482"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950482/Effects_of_Diallyl_Trisulfide_on_TNF_%CE%B1_stimulated_Genetically_different_Triple_Negative_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Effects of Diallyl Trisulfide on TNF‐α‐stimulated Genetically different Triple‐Negative Breast Cancer Cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950482/Effects_of_Diallyl_Trisulfide_on_TNF_%CE%B1_stimulated_Genetically_different_Triple_Negative_Breast_Cancer_Cells">Effects of Diallyl Trisulfide on TNF‐α‐stimulated Genetically different Triple‐Negative Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>The FASEB Journal</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950482"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950482"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950482; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950482]").text(description); $(".js-view-count[data-work-id=124950482]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950482; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950482']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950482]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950482,"title":"Effects of Diallyl Trisulfide on TNF‐α‐stimulated Genetically different Triple‐Negative Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Wiley","publication_name":"The FASEB Journal"},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950482/Effects_of_Diallyl_Trisulfide_on_TNF_%CE%B1_stimulated_Genetically_different_Triple_Negative_Breast_Cancer_Cells","translated_internal_url":"","created_at":"2024-10-22T08:29:17.778-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Effects_of_Diallyl_Trisulfide_on_TNF_α_stimulated_Genetically_different_Triple_Negative_Breast_Cancer_Cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":32723,"name":"Angiogenesis","url":"https://www.academia.edu/Documents/in/Angiogenesis"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"},{"id":295234,"name":"Chemokine","url":"https://www.academia.edu/Documents/in/Chemokine"},{"id":1461942,"name":"CCL","url":"https://www.academia.edu/Documents/in/CCL"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950481"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950481/Prognostic_Relevance_of_ZNF844_and_Chr_19p13_2_KRAB_Zinc_Finger_Proteins_in_Clear_Cell_Renal_Carcinoma"><img alt="Research paper thumbnail of Prognostic Relevance of ZNF844 and Chr 19p13.2 KRAB-Zinc Finger Proteins in Clear Cell Renal Carcinoma" class="work-thumbnail" src="https://attachments.academia-assets.com/119081018/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950481/Prognostic_Relevance_of_ZNF844_and_Chr_19p13_2_KRAB_Zinc_Finger_Proteins_in_Clear_Cell_Renal_Carcinoma">Prognostic Relevance of ZNF844 and Chr 19p13.2 KRAB-Zinc Finger Proteins in Clear Cell Renal Carcinoma</a></div><div class="wp-workCard_item"><span>Cancer Genomics - Proteomics</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background/Aim: Clear-cell renal cell carcinoma (ccRCC) is the most common and aggressive form of...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background/Aim: Clear-cell renal cell carcinoma (ccRCC) is the most common and aggressive form of all urological cancers, with poor prognosis and high mortality. Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. KRAB Zinc finger proteins (KRAB-ZFPs) are the largest family of mammalian transcription regulators. They are differentially expressed in various tissues during cellular development and phenotypic differentiation. Materials and Methods: In this study, the levels of transcripts of ccRCC from The Cancer Genome Atlas (TCGA) dataset were used to identify prognostic biomarkers in this disease. Results: Using bioinformatics techniques, we demonstrate that approximately 60% of KRAB zinc finger proteins located on chromosome 19p13.2 are differentially expressed, with all but two being down-regulated in ccRCC. Moreover, ZNF844, a paralog of ZNF433, was the most down-regulated across all histological grades and pathological stages (p<0.001). In addition, the decrease in ZNF844 expression was associated with poor patient survival (HR=0.41; 95% CI=0.3-0.56; p<0.0001). Gene Set Enrichment Analysis of genes inversely co-expressed with ZNF844 revealed that enriched pathways were consistently related to immune and translation processes (p<0.05, FDR <0.05). Lastly, ZNF844 expression showed moderate, inverse correlation to Helper Tcell (CD4 or Th1) subtype 1 (R=-0.558, p=5.15×10-39) infiltration and with the exhausted T-cell phenotype (R=-0.37; p=4.1×10-21). Conclusion: Down-regulation of KRAB-ZFPs at 19p13.2 may represent a signature for ccRCC. Moreover, ZNF844 is a prognostic marker for ccRCC and may serve as a putative immune-related tumor suppressor gene. Clear cell renal carcinoma (ccRCC) is the most common neoplastic disease affecting the kidneys. It accounts for at least 70% of all kidney cancers (1, 2). In advanced stages, ccRCC becomes resistant to conventional therapies (1-3). Moreover, later stages are associated with poor prognosis with a 5-year overall survival rate of less than 10% (1-3). Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. Kruppel-associated box domain-containing zinc-finger proteins (KRAB-ZFP) represent the most prominent family of transcriptional repressors (4, 5). The human genome contains over 300 KRAB-ZFPs genes that produce more than 800 transcripts that encode proteins, pseudogenes, and splice variants (6-8). KRAB-ZFPs are differentially expressed in various tissues during cellular development. Several of these genes are involved in embryogenesis, genome imprinting, and biological processes that determine phenotypes in stem cells (9-11). Given their roles in cellular differentiation and their ability to alter gene expression via epigenetic processes and chromatin remodeling, it is conceivable that dysregulation of KRAB-ZFP transcription factors could facilitate tumorigenesis and tumor progression. Interestingly, several large KRAB-ZFP clusters are located on chromosome 19 (chr19), and several studies have linked genetic alterations in chromosome 19p13 to cancers (12-18). Using data mining techniques, we recently identified ZNF433, a zinc finger that is differentially expressed in ccRCC (19) and that may be a biomarker for ccRCC. ZNF433 is part of a cluster of KRAB-ZFPs that are located on chromosome 19p13.2. Thus, we focused on this locus to ascertain if the expression of other members of this cluster was altered. We have identified several KRAB-ZFPs that are differentially expressed and are associated with changes in overall survival in patients. Since the gene ZNF844 is a paralog of ZNF433, it appears to be a strong candidate biomarker and prognostic factor for ccRCC. 305</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="cc8cab3d0a99851de4db3c74eaa79c04" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081018,"asset_id":124950481,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081018/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950481"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950481"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950481; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950481]").text(description); $(".js-view-count[data-work-id=124950481]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950481; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950481']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "cc8cab3d0a99851de4db3c74eaa79c04" } } $('.js-work-strip[data-work-id=124950481]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950481,"title":"Prognostic Relevance of ZNF844 and Chr 19p13.2 KRAB-Zinc Finger Proteins in Clear Cell Renal Carcinoma","translated_title":"","metadata":{"publisher":"Anticancer Research USA Inc.","grobid_abstract":"Background/Aim: Clear-cell renal cell carcinoma (ccRCC) is the most common and aggressive form of all urological cancers, with poor prognosis and high mortality. Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. KRAB Zinc finger proteins (KRAB-ZFPs) are the largest family of mammalian transcription regulators. They are differentially expressed in various tissues during cellular development and phenotypic differentiation. Materials and Methods: In this study, the levels of transcripts of ccRCC from The Cancer Genome Atlas (TCGA) dataset were used to identify prognostic biomarkers in this disease. Results: Using bioinformatics techniques, we demonstrate that approximately 60% of KRAB zinc finger proteins located on chromosome 19p13.2 are differentially expressed, with all but two being down-regulated in ccRCC. Moreover, ZNF844, a paralog of ZNF433, was the most down-regulated across all histological grades and pathological stages (p\u003c0.001). In addition, the decrease in ZNF844 expression was associated with poor patient survival (HR=0.41; 95% CI=0.3-0.56; p\u003c0.0001). Gene Set Enrichment Analysis of genes inversely co-expressed with ZNF844 revealed that enriched pathways were consistently related to immune and translation processes (p\u003c0.05, FDR \u003c0.05). Lastly, ZNF844 expression showed moderate, inverse correlation to Helper Tcell (CD4 or Th1) subtype 1 (R=-0.558, p=5.15×10-39) infiltration and with the exhausted T-cell phenotype (R=-0.37; p=4.1×10-21). Conclusion: Down-regulation of KRAB-ZFPs at 19p13.2 may represent a signature for ccRCC. Moreover, ZNF844 is a prognostic marker for ccRCC and may serve as a putative immune-related tumor suppressor gene. Clear cell renal carcinoma (ccRCC) is the most common neoplastic disease affecting the kidneys. It accounts for at least 70% of all kidney cancers (1, 2). In advanced stages, ccRCC becomes resistant to conventional therapies (1-3). Moreover, later stages are associated with poor prognosis with a 5-year overall survival rate of less than 10% (1-3). Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. Kruppel-associated box domain-containing zinc-finger proteins (KRAB-ZFP) represent the most prominent family of transcriptional repressors (4, 5). The human genome contains over 300 KRAB-ZFPs genes that produce more than 800 transcripts that encode proteins, pseudogenes, and splice variants (6-8). KRAB-ZFPs are differentially expressed in various tissues during cellular development. Several of these genes are involved in embryogenesis, genome imprinting, and biological processes that determine phenotypes in stem cells (9-11). Given their roles in cellular differentiation and their ability to alter gene expression via epigenetic processes and chromatin remodeling, it is conceivable that dysregulation of KRAB-ZFP transcription factors could facilitate tumorigenesis and tumor progression. Interestingly, several large KRAB-ZFP clusters are located on chromosome 19 (chr19), and several studies have linked genetic alterations in chromosome 19p13 to cancers (12-18). Using data mining techniques, we recently identified ZNF433, a zinc finger that is differentially expressed in ccRCC (19) and that may be a biomarker for ccRCC. ZNF433 is part of a cluster of KRAB-ZFPs that are located on chromosome 19p13.2. Thus, we focused on this locus to ascertain if the expression of other members of this cluster was altered. We have identified several KRAB-ZFPs that are differentially expressed and are associated with changes in overall survival in patients. Since the gene ZNF844 is a paralog of ZNF433, it appears to be a strong candidate biomarker and prognostic factor for ccRCC. 305","publication_name":"Cancer Genomics - Proteomics","grobid_abstract_attachment_id":119081018},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950481/Prognostic_Relevance_of_ZNF844_and_Chr_19p13_2_KRAB_Zinc_Finger_Proteins_in_Clear_Cell_Renal_Carcinoma","translated_internal_url":"","created_at":"2024-10-22T08:29:17.497-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081018,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081018/thumbnails/1.jpg","file_name":"305.full.pdf","download_url":"https://www.academia.edu/attachments/119081018/download_file","bulk_download_file_name":"Prognostic_Relevance_of_ZNF844_and_Chr_1.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081018/305.full-libre.pdf?1729611567=\u0026response-content-disposition=attachment%3B+filename%3DPrognostic_Relevance_of_ZNF844_and_Chr_1.pdf\u0026Expires=1742120023\u0026Signature=WmWPVa4IHkvH6takCTGYu8MogJoEi6X0EO40AWBEBXZuaXAlecN3RVy~QNfHN~mlRXGtzNi8jMuwwtvg7rHmUOgvmuWlae4l4W8L-pSQRICRQiyrChoJe34BeTsjrLkNu6MaeBsQ7tB65E~GZJ3gO0viFD~ixC2rv1CwZ~qZpKVF6ZjkKD60GsoMWSHS80RW5cuy86xfJCxJz0LCM0uGW-uSABTecI4oYYsil4B9XXG4hCO3S3c7vRebgReSoOwPmDnxn17U6nkaJRwyw9ystpi19vxIGyVeVDZn9fjotAcEdx7HhAFmAaR4QvtmjEODX4kg~eP7wDp6BNNgbOFMFA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Prognostic_Relevance_of_ZNF844_and_Chr_19p13_2_KRAB_Zinc_Finger_Proteins_in_Clear_Cell_Renal_Carcinoma","translated_slug":"","page_count":23,"language":"en","content_type":"Work","summary":"Background/Aim: Clear-cell renal cell carcinoma (ccRCC) is the most common and aggressive form of all urological cancers, with poor prognosis and high mortality. Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. KRAB Zinc finger proteins (KRAB-ZFPs) are the largest family of mammalian transcription regulators. They are differentially expressed in various tissues during cellular development and phenotypic differentiation. Materials and Methods: In this study, the levels of transcripts of ccRCC from The Cancer Genome Atlas (TCGA) dataset were used to identify prognostic biomarkers in this disease. Results: Using bioinformatics techniques, we demonstrate that approximately 60% of KRAB zinc finger proteins located on chromosome 19p13.2 are differentially expressed, with all but two being down-regulated in ccRCC. Moreover, ZNF844, a paralog of ZNF433, was the most down-regulated across all histological grades and pathological stages (p\u003c0.001). In addition, the decrease in ZNF844 expression was associated with poor patient survival (HR=0.41; 95% CI=0.3-0.56; p\u003c0.0001). Gene Set Enrichment Analysis of genes inversely co-expressed with ZNF844 revealed that enriched pathways were consistently related to immune and translation processes (p\u003c0.05, FDR \u003c0.05). Lastly, ZNF844 expression showed moderate, inverse correlation to Helper Tcell (CD4 or Th1) subtype 1 (R=-0.558, p=5.15×10-39) infiltration and with the exhausted T-cell phenotype (R=-0.37; p=4.1×10-21). Conclusion: Down-regulation of KRAB-ZFPs at 19p13.2 may represent a signature for ccRCC. Moreover, ZNF844 is a prognostic marker for ccRCC and may serve as a putative immune-related tumor suppressor gene. Clear cell renal carcinoma (ccRCC) is the most common neoplastic disease affecting the kidneys. It accounts for at least 70% of all kidney cancers (1, 2). In advanced stages, ccRCC becomes resistant to conventional therapies (1-3). Moreover, later stages are associated with poor prognosis with a 5-year overall survival rate of less than 10% (1-3). Despite growing evidence of involvement in carcinogenesis, the role of KRAB-ZFP in ccRCC has not been fully explored. Kruppel-associated box domain-containing zinc-finger proteins (KRAB-ZFP) represent the most prominent family of transcriptional repressors (4, 5). The human genome contains over 300 KRAB-ZFPs genes that produce more than 800 transcripts that encode proteins, pseudogenes, and splice variants (6-8). KRAB-ZFPs are differentially expressed in various tissues during cellular development. Several of these genes are involved in embryogenesis, genome imprinting, and biological processes that determine phenotypes in stem cells (9-11). Given their roles in cellular differentiation and their ability to alter gene expression via epigenetic processes and chromatin remodeling, it is conceivable that dysregulation of KRAB-ZFP transcription factors could facilitate tumorigenesis and tumor progression. Interestingly, several large KRAB-ZFP clusters are located on chromosome 19 (chr19), and several studies have linked genetic alterations in chromosome 19p13 to cancers (12-18). Using data mining techniques, we recently identified ZNF433, a zinc finger that is differentially expressed in ccRCC (19) and that may be a biomarker for ccRCC. ZNF433 is part of a cluster of KRAB-ZFPs that are located on chromosome 19p13.2. Thus, we focused on this locus to ascertain if the expression of other members of this cluster was altered. We have identified several KRAB-ZFPs that are differentially expressed and are associated with changes in overall survival in patients. Since the gene ZNF844 is a paralog of ZNF433, it appears to be a strong candidate biomarker and prognostic factor for ccRCC. 305","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081018,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081018/thumbnails/1.jpg","file_name":"305.full.pdf","download_url":"https://www.academia.edu/attachments/119081018/download_file","bulk_download_file_name":"Prognostic_Relevance_of_ZNF844_and_Chr_1.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081018/305.full-libre.pdf?1729611567=\u0026response-content-disposition=attachment%3B+filename%3DPrognostic_Relevance_of_ZNF844_and_Chr_1.pdf\u0026Expires=1742120023\u0026Signature=WmWPVa4IHkvH6takCTGYu8MogJoEi6X0EO40AWBEBXZuaXAlecN3RVy~QNfHN~mlRXGtzNi8jMuwwtvg7rHmUOgvmuWlae4l4W8L-pSQRICRQiyrChoJe34BeTsjrLkNu6MaeBsQ7tB65E~GZJ3gO0viFD~ixC2rv1CwZ~qZpKVF6ZjkKD60GsoMWSHS80RW5cuy86xfJCxJz0LCM0uGW-uSABTecI4oYYsil4B9XXG4hCO3S3c7vRebgReSoOwPmDnxn17U6nkaJRwyw9ystpi19vxIGyVeVDZn9fjotAcEdx7HhAFmAaR4QvtmjEODX4kg~eP7wDp6BNNgbOFMFA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":1290,"name":"Immunology","url":"https://www.academia.edu/Documents/in/Immunology"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":105308,"name":"Renal cell Carcinoma","url":"https://www.academia.edu/Documents/in/Renal_cell_Carcinoma"},{"id":201737,"name":"Clear Cell Renal Cell Carcinoma","url":"https://www.academia.edu/Documents/in/Clear_Cell_Renal_Cell_Carcinoma"},{"id":213897,"name":"Phenotype","url":"https://www.academia.edu/Documents/in/Phenotype"},{"id":213901,"name":"Transcription Factor","url":"https://www.academia.edu/Documents/in/Transcription_Factor"},{"id":329425,"name":"Zinc Finger","url":"https://www.academia.edu/Documents/in/Zinc_Finger"},{"id":340262,"name":"Carcinogenesis","url":"https://www.academia.edu/Documents/in/Carcinogenesis"}],"urls":[{"id":45280618,"url":"https://syndication.highwire.org/content/doi/10.21873/cgp.20322"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950480"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950480/Anaerobic_glycolysis_and_ATP_production_after_complex_I_inhibition_by_MPP_in_C_6_glioma_cells"><img alt="Research paper thumbnail of Anaerobic glycolysis and ATP production after complex I inhibition by MPP+ in C‐6 glioma cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950480/Anaerobic_glycolysis_and_ATP_production_after_complex_I_inhibition_by_MPP_in_C_6_glioma_cells">Anaerobic glycolysis and ATP production after complex I inhibition by MPP+ in C‐6 glioma cells</a></div><div class="wp-workCard_item"><span>The FASEB Journal</span><span>, 2006</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950480"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950480"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950480; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950480]").text(description); $(".js-view-count[data-work-id=124950480]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950480; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950480']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950480]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950480,"title":"Anaerobic glycolysis and ATP production after complex I inhibition by MPP+ in C‐6 glioma cells","translated_title":"","metadata":{"publisher":"Wiley","publication_date":{"day":null,"month":null,"year":2006,"errors":{}},"publication_name":"The FASEB Journal"},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950480/Anaerobic_glycolysis_and_ATP_production_after_complex_I_inhibition_by_MPP_in_C_6_glioma_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:17.298-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Anaerobic_glycolysis_and_ATP_production_after_complex_I_inhibition_by_MPP_in_C_6_glioma_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":61714,"name":"Production economics","url":"https://www.academia.edu/Documents/in/Production_economics"},{"id":76383,"name":"Glioma","url":"https://www.academia.edu/Documents/in/Glioma"},{"id":172897,"name":"Glycolysis","url":"https://www.academia.edu/Documents/in/Glycolysis"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":389302,"name":"Anaerobic Exercise","url":"https://www.academia.edu/Documents/in/Anaerobic_Exercise"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2761404,"name":"anaerobic glycolysis","url":"https://www.academia.edu/Documents/in/anaerobic_glycolysis"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950479"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950479/Hypoxia_Hyperoxia_or_pH_Predominant_Factors_in_Tumor_Cell_Survival"><img alt="Research paper thumbnail of Hypoxia, Hyperoxia or pH ? Predominant Factors in Tumor Cell Survival" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950479/Hypoxia_Hyperoxia_or_pH_Predominant_Factors_in_Tumor_Cell_Survival">Hypoxia, Hyperoxia or pH ? Predominant Factors in Tumor Cell Survival</a></div><div class="wp-workCard_item"><span>The FASEB Journal</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experi...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experimental conditions that do not control for the shift in pH.MethodsHere, we examine the molecular genetic effects of (~91% O2 (hyperoxia) vs. ~2.5% O2 (hypoxia)) at a uniform pH ~7.2 using microarrays, HPLC, imaging probes and Western blot.ResultsHyperoxic and Hypoxic culture conditions for 24 hrs had no adverse effect on viability in malignant N2a cells, provided pH was neutral with ample glucose supply. The hyperoxic transcriptome showed elevation of mRNA of 42 mitochondrial genes, DNA/base excision repair, G protein signaling, protein synthesis, transcription and ubiquitin‐mediated proteolysis. The hypoxic transcriptome corresponded to major elevations in epigenetic (lysine (K)‐specific demethylases, H4k/d/j, Hist4h4, Hist2h3c1, Rara and REST corepressor 2) with greater expression of protein/mRNA for solute carrier family 16, member 3 MCT‐4 (lactate transporter). Blocking MCT‐4 (phloret...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950479"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950479"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950479; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950479]").text(description); $(".js-view-count[data-work-id=124950479]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950479; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950479']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950479]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950479,"title":"Hypoxia, Hyperoxia or pH ? Predominant Factors in Tumor Cell Survival","translated_title":"","metadata":{"abstract":"BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experimental conditions that do not control for the shift in pH.MethodsHere, we examine the molecular genetic effects of (~91% O2 (hyperoxia) vs. ~2.5% O2 (hypoxia)) at a uniform pH ~7.2 using microarrays, HPLC, imaging probes and Western blot.ResultsHyperoxic and Hypoxic culture conditions for 24 hrs had no adverse effect on viability in malignant N2a cells, provided pH was neutral with ample glucose supply. The hyperoxic transcriptome showed elevation of mRNA of 42 mitochondrial genes, DNA/base excision repair, G protein signaling, protein synthesis, transcription and ubiquitin‐mediated proteolysis. The hypoxic transcriptome corresponded to major elevations in epigenetic (lysine (K)‐specific demethylases, H4k/d/j, Hist4h4, Hist2h3c1, Rara and REST corepressor 2) with greater expression of protein/mRNA for solute carrier family 16, member 3 MCT‐4 (lactate transporter). Blocking MCT‐4 (phloret...","publisher":"Wiley","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"The FASEB Journal"},"translated_abstract":"BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experimental conditions that do not control for the shift in pH.MethodsHere, we examine the molecular genetic effects of (~91% O2 (hyperoxia) vs. ~2.5% O2 (hypoxia)) at a uniform pH ~7.2 using microarrays, HPLC, imaging probes and Western blot.ResultsHyperoxic and Hypoxic culture conditions for 24 hrs had no adverse effect on viability in malignant N2a cells, provided pH was neutral with ample glucose supply. The hyperoxic transcriptome showed elevation of mRNA of 42 mitochondrial genes, DNA/base excision repair, G protein signaling, protein synthesis, transcription and ubiquitin‐mediated proteolysis. The hypoxic transcriptome corresponded to major elevations in epigenetic (lysine (K)‐specific demethylases, H4k/d/j, Hist4h4, Hist2h3c1, Rara and REST corepressor 2) with greater expression of protein/mRNA for solute carrier family 16, member 3 MCT‐4 (lactate transporter). Blocking MCT‐4 (phloret...","internal_url":"https://www.academia.edu/124950479/Hypoxia_Hyperoxia_or_pH_Predominant_Factors_in_Tumor_Cell_Survival","translated_internal_url":"","created_at":"2024-10-22T08:29:17.047-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Hypoxia_Hyperoxia_or_pH_Predominant_Factors_in_Tumor_Cell_Survival","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"BackgroundThe study of hyperoxia vs. hypoxia on tumor cell survival is often studied under experimental conditions that do not control for the shift in pH.MethodsHere, we examine the molecular genetic effects of (~91% O2 (hyperoxia) vs. ~2.5% O2 (hypoxia)) at a uniform pH ~7.2 using microarrays, HPLC, imaging probes and Western blot.ResultsHyperoxic and Hypoxic culture conditions for 24 hrs had no adverse effect on viability in malignant N2a cells, provided pH was neutral with ample glucose supply. The hyperoxic transcriptome showed elevation of mRNA of 42 mitochondrial genes, DNA/base excision repair, G protein signaling, protein synthesis, transcription and ubiquitin‐mediated proteolysis. The hypoxic transcriptome corresponded to major elevations in epigenetic (lysine (K)‐specific demethylases, H4k/d/j, Hist4h4, Hist2h3c1, Rara and REST corepressor 2) with greater expression of protein/mRNA for solute carrier family 16, member 3 MCT‐4 (lactate transporter). Blocking MCT‐4 (phloret...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":167,"name":"Physiology","url":"https://www.academia.edu/Documents/in/Physiology"},{"id":2513,"name":"Molecular Biology","url":"https://www.academia.edu/Documents/in/Molecular_Biology"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":43761,"name":"Transcriptome","url":"https://www.academia.edu/Documents/in/Transcriptome"},{"id":186234,"name":"Medical Physiology","url":"https://www.academia.edu/Documents/in/Medical_Physiology"},{"id":995532,"name":"Hyperoxia","url":"https://www.academia.edu/Documents/in/Hyperoxia"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950478"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950478/Cocaine_potentiates_an_inflammatory_response_in_C6_astroglia_like_cells"><img alt="Research paper thumbnail of Cocaine potentiates an inflammatory response in C6 astroglia‑like cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081012/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950478/Cocaine_potentiates_an_inflammatory_response_in_C6_astroglia_like_cells">Cocaine potentiates an inflammatory response in C6 astroglia‑like cells</a></div><div class="wp-workCard_item"><span>Biomedical Reports</span><span>, 2021</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">cells at higher cocaine doses compared with the unchallenged cells. Since high concentrations of ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">cells at higher cocaine doses compared with the unchallenged cells. Since high concentrations of NO are associated with inflammation, the high levels of NO production observed in the present study suggested that cocaine may have potentiated the inflammatory response in the challenged C6 astroglia-like cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7e6cf18923902df8b053cd1db455c979" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081012,"asset_id":124950478,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081012/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950478"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950478"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950478; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950478]").text(description); $(".js-view-count[data-work-id=124950478]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950478; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950478']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "7e6cf18923902df8b053cd1db455c979" } } $('.js-work-strip[data-work-id=124950478]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950478,"title":"Cocaine potentiates an inflammatory response in C6 astroglia‑like cells","translated_title":"","metadata":{"publisher":"Spandidos Publications","grobid_abstract":"cells at higher cocaine doses compared with the unchallenged cells. Since high concentrations of NO are associated with inflammation, the high levels of NO production observed in the present study suggested that cocaine may have potentiated the inflammatory response in the challenged C6 astroglia-like cells.","publication_date":{"day":null,"month":null,"year":2021,"errors":{}},"publication_name":"Biomedical Reports","grobid_abstract_attachment_id":119081012},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950478/Cocaine_potentiates_an_inflammatory_response_in_C6_astroglia_like_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:16.684-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081012,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081012/thumbnails/1.jpg","file_name":"download.pdf","download_url":"https://www.academia.edu/attachments/119081012/download_file","bulk_download_file_name":"Cocaine_potentiates_an_inflammatory_resp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081012/download-libre.pdf?1729611323=\u0026response-content-disposition=attachment%3B+filename%3DCocaine_potentiates_an_inflammatory_resp.pdf\u0026Expires=1742120023\u0026Signature=NfwKGXH3K2JBK~VFCgRUCBLlS9nCKngORutSOSfyZYIAEYRuYb3O7zRy1T8kZ5WSKnBfqvsjT8rJqE9S4r2dW~nN9MPdkUdgpx---DSKo~QMrMDFjU-cdmuQDHP-vMt-1dC9D176ZU5uYUkpLSzXi4HfViEE~VEsZpBF4IQCUE1TEaE1BKnGfQKdYHw6ECghA97zkbPPyQ-s8KciNrj62p83VBV1qaROYlHUD4ibVh0GGIC~41VfGL-RvfgtwClcWE13aRm~2qy5hHwOb6TA9CEtjr4lTDjxl3GShEuWBz2kdbwbrOIbNbEVLHeISk8NoDhUc1FY~5M5IsnNlr3okQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Cocaine_potentiates_an_inflammatory_response_in_C6_astroglia_like_cells","translated_slug":"","page_count":7,"language":"en","content_type":"Work","summary":"cells at higher cocaine doses compared with the unchallenged cells. Since high concentrations of NO are associated with inflammation, the high levels of NO production observed in the present study suggested that cocaine may have potentiated the inflammatory response in the challenged C6 astroglia-like cells.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081012,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081012/thumbnails/1.jpg","file_name":"download.pdf","download_url":"https://www.academia.edu/attachments/119081012/download_file","bulk_download_file_name":"Cocaine_potentiates_an_inflammatory_resp.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081012/download-libre.pdf?1729611323=\u0026response-content-disposition=attachment%3B+filename%3DCocaine_potentiates_an_inflammatory_resp.pdf\u0026Expires=1742120023\u0026Signature=NfwKGXH3K2JBK~VFCgRUCBLlS9nCKngORutSOSfyZYIAEYRuYb3O7zRy1T8kZ5WSKnBfqvsjT8rJqE9S4r2dW~nN9MPdkUdgpx---DSKo~QMrMDFjU-cdmuQDHP-vMt-1dC9D176ZU5uYUkpLSzXi4HfViEE~VEsZpBF4IQCUE1TEaE1BKnGfQKdYHw6ECghA97zkbPPyQ-s8KciNrj62p83VBV1qaROYlHUD4ibVh0GGIC~41VfGL-RvfgtwClcWE13aRm~2qy5hHwOb6TA9CEtjr4lTDjxl3GShEuWBz2kdbwbrOIbNbEVLHeISk8NoDhUc1FY~5M5IsnNlr3okQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":140,"name":"Pharmacology","url":"https://www.academia.edu/Documents/in/Pharmacology"},{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":48183,"name":"Lipopolysaccharide","url":"https://www.academia.edu/Documents/in/Lipopolysaccharide"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950477"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950477/Effect_of_Diallyl_Trisulfide_on_TNF_%CE%B1_induced_CCL2_MCP_1_Release_in_Genetically_Different_Triple_negative_Breast_Cancer_Cells"><img alt="Research paper thumbnail of Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081015/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950477/Effect_of_Diallyl_Trisulfide_on_TNF_%CE%B1_induced_CCL2_MCP_1_Release_in_Genetically_Different_Triple_negative_Breast_Cancer_Cells">Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells</a></div><div class="wp-workCard_item"><span>Anticancer Research</span><span>, 2021</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit breast carcinogen...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit breast carcinogenesis. CCL2/MCP-1 has been shown to play a significant role in breast cancer. This study explored DATS efficacy on triple-negative breast cancer (TNBC) cells. Materials and Methods: DATS efficacy on TNFα induced TNBC cells were examined via trypan blue exclusion test, wound-healing assay, human cytokine arrays, ELISA, and RT-PCR. Results: DATS significantly induced cell death and inhibited cell migration. Expression of CCL2/MCP-1, IL-6, PDGF-BB, NT-3, and GM-CSF in TNF-α-treated cells increased. However, DATS significantly decreased the expression of CCL2/MCP-1 in TNF-α-treated MDA-MB-231 but not in MDA-MB-468 cells. DATS significantly down-regulated mRNA expression of IKBKE and MAPK8 in both cell lines, indicating a possible effect in genes involved in the NF-ĸB and MAPK signaling. Conclusion: DATS may have a role in TNBC therapy and prevention by targeting CCL2.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f57cd9a30ef121ff634af43a91426ab7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081015,"asset_id":124950477,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081015/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950477"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950477"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950477; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950477]").text(description); $(".js-view-count[data-work-id=124950477]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950477; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950477']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "f57cd9a30ef121ff634af43a91426ab7" } } $('.js-work-strip[data-work-id=124950477]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950477,"title":"Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells","translated_title":"","metadata":{"publisher":"Anticancer Research USA Inc.","grobid_abstract":"Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit breast carcinogenesis. CCL2/MCP-1 has been shown to play a significant role in breast cancer. This study explored DATS efficacy on triple-negative breast cancer (TNBC) cells. Materials and Methods: DATS efficacy on TNFα induced TNBC cells were examined via trypan blue exclusion test, wound-healing assay, human cytokine arrays, ELISA, and RT-PCR. Results: DATS significantly induced cell death and inhibited cell migration. Expression of CCL2/MCP-1, IL-6, PDGF-BB, NT-3, and GM-CSF in TNF-α-treated cells increased. However, DATS significantly decreased the expression of CCL2/MCP-1 in TNF-α-treated MDA-MB-231 but not in MDA-MB-468 cells. DATS significantly down-regulated mRNA expression of IKBKE and MAPK8 in both cell lines, indicating a possible effect in genes involved in the NF-ĸB and MAPK signaling. Conclusion: DATS may have a role in TNBC therapy and prevention by targeting CCL2.","publication_date":{"day":null,"month":null,"year":2021,"errors":{}},"publication_name":"Anticancer Research","grobid_abstract_attachment_id":119081015},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950477/Effect_of_Diallyl_Trisulfide_on_TNF_%CE%B1_induced_CCL2_MCP_1_Release_in_Genetically_Different_Triple_negative_Breast_Cancer_Cells","translated_internal_url":"","created_at":"2024-10-22T08:29:16.439-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081015,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081015/thumbnails/1.jpg","file_name":"5919.full.pdf","download_url":"https://www.academia.edu/attachments/119081015/download_file","bulk_download_file_name":"Effect_of_Diallyl_Trisulfide_on_TNF__in.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081015/5919.full-libre.pdf?1729611354=\u0026response-content-disposition=attachment%3B+filename%3DEffect_of_Diallyl_Trisulfide_on_TNF__in.pdf\u0026Expires=1742120023\u0026Signature=ch3H9S4TLVr~b-Qa5M53PyW19UZZ6pV4URTR1KHDtM9jMzck3kwcTy6AvseF5vFhGQnfiBAg8H2MvXKvMwSD9xkC1qOwYxcLXTVbIuLEDBaD8xmfHfFF5nwP0hN9UqucaDL0A1P7W1QsX-sP18fQbA8~h3YHi1bT4g5WUgWpp9cT~f2QD3x5nzOnYoojUP-4dw86URpBD6phdICkVVSgYSMp53h6N8XfOzn71NVsr7VBDdzh4euqnaws5XyE0MXu9LWCVQ1ZrQL5cEPawoDLinroanvaNx-1mH3wm2dRUvaptZddi~SjpD7qNpHv-K80OgIw2Ht~sPlp4Ecga7DDaQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Effect_of_Diallyl_Trisulfide_on_TNF_α_induced_CCL2_MCP_1_Release_in_Genetically_Different_Triple_negative_Breast_Cancer_Cells","translated_slug":"","page_count":15,"language":"en","content_type":"Work","summary":"Background/Aim: Diallyl trisulfide (DATS) has been shown to prevent and inhibit breast carcinogenesis. CCL2/MCP-1 has been shown to play a significant role in breast cancer. This study explored DATS efficacy on triple-negative breast cancer (TNBC) cells. Materials and Methods: DATS efficacy on TNFα induced TNBC cells were examined via trypan blue exclusion test, wound-healing assay, human cytokine arrays, ELISA, and RT-PCR. Results: DATS significantly induced cell death and inhibited cell migration. Expression of CCL2/MCP-1, IL-6, PDGF-BB, NT-3, and GM-CSF in TNF-α-treated cells increased. However, DATS significantly decreased the expression of CCL2/MCP-1 in TNF-α-treated MDA-MB-231 but not in MDA-MB-468 cells. DATS significantly down-regulated mRNA expression of IKBKE and MAPK8 in both cell lines, indicating a possible effect in genes involved in the NF-ĸB and MAPK signaling. Conclusion: DATS may have a role in TNBC therapy and prevention by targeting CCL2.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081015,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081015/thumbnails/1.jpg","file_name":"5919.full.pdf","download_url":"https://www.academia.edu/attachments/119081015/download_file","bulk_download_file_name":"Effect_of_Diallyl_Trisulfide_on_TNF__in.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081015/5919.full-libre.pdf?1729611354=\u0026response-content-disposition=attachment%3B+filename%3DEffect_of_Diallyl_Trisulfide_on_TNF__in.pdf\u0026Expires=1742120023\u0026Signature=ch3H9S4TLVr~b-Qa5M53PyW19UZZ6pV4URTR1KHDtM9jMzck3kwcTy6AvseF5vFhGQnfiBAg8H2MvXKvMwSD9xkC1qOwYxcLXTVbIuLEDBaD8xmfHfFF5nwP0hN9UqucaDL0A1P7W1QsX-sP18fQbA8~h3YHi1bT4g5WUgWpp9cT~f2QD3x5nzOnYoojUP-4dw86URpBD6phdICkVVSgYSMp53h6N8XfOzn71NVsr7VBDdzh4euqnaws5XyE0MXu9LWCVQ1ZrQL5cEPawoDLinroanvaNx-1mH3wm2dRUvaptZddi~SjpD7qNpHv-K80OgIw2Ht~sPlp4Ecga7DDaQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":263843,"name":"Anticancer","url":"https://www.academia.edu/Documents/in/Anticancer"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"},{"id":376275,"name":"Trypan Blue","url":"https://www.academia.edu/Documents/in/Trypan_Blue"},{"id":474029,"name":"Tumor necrosis factor-alpha","url":"https://www.academia.edu/Documents/in/Tumor_necrosis_factor-alpha"},{"id":1461942,"name":"CCL","url":"https://www.academia.edu/Documents/in/CCL"}],"urls":[{"id":45280617,"url":"https://syndication.highwire.org/content/doi/10.21873/anticanres.15411"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950476"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/124950476/Epigenetic_Patterns_Therapies_Associated_with_Genetic_Disorders"><img alt="Research paper thumbnail of Epigenetic Patterns/Therapies Associated with Genetic Disorders" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/124950476/Epigenetic_Patterns_Therapies_Associated_with_Genetic_Disorders">Epigenetic Patterns/Therapies Associated with Genetic Disorders</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Within the past three centuries, all-cause disease burden in developed countries has shifted from...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Within the past three centuries, all-cause disease burden in developed countries has shifted from infectious to non-communicable (NCD)/genetic based diseases including cardiovascular conditions, cancer, neuropsychiatric conditions, and diabetes. Factors accounting for this drift include discoveries in vaccination (e.g., tetanus, cholera, typhoid, plague, anthrax, and tuberculosis), antibiotics, advances in medical diagnostics, lasers, surgical techniques, and routine medicines to treat almost every type of systemic imbalance. Moreover, advances in public health, sanitation, food safety, and geriatric sciences are creating extended life expectancy, where age-related illnesses (osteoarthritis, back pain, neurodegenerative conditions) in addition to NCDs are plaguing an ever-growing elderly population. The age-related risk for these diseases is now worsened by aggregation of global industrial pollutants, where the World Health Organization (WHO) now uses the term “environmental burden ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950476"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950476"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950476; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950476]").text(description); $(".js-view-count[data-work-id=124950476]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950476; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950476']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=124950476]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950476,"title":"Epigenetic Patterns/Therapies Associated with Genetic Disorders","translated_title":"","metadata":{"abstract":"Within the past three centuries, all-cause disease burden in developed countries has shifted from infectious to non-communicable (NCD)/genetic based diseases including cardiovascular conditions, cancer, neuropsychiatric conditions, and diabetes. Factors accounting for this drift include discoveries in vaccination (e.g., tetanus, cholera, typhoid, plague, anthrax, and tuberculosis), antibiotics, advances in medical diagnostics, lasers, surgical techniques, and routine medicines to treat almost every type of systemic imbalance. Moreover, advances in public health, sanitation, food safety, and geriatric sciences are creating extended life expectancy, where age-related illnesses (osteoarthritis, back pain, neurodegenerative conditions) in addition to NCDs are plaguing an ever-growing elderly population. The age-related risk for these diseases is now worsened by aggregation of global industrial pollutants, where the World Health Organization (WHO) now uses the term “environmental burden ...","publication_date":{"day":null,"month":null,"year":2018,"errors":{}}},"translated_abstract":"Within the past three centuries, all-cause disease burden in developed countries has shifted from infectious to non-communicable (NCD)/genetic based diseases including cardiovascular conditions, cancer, neuropsychiatric conditions, and diabetes. Factors accounting for this drift include discoveries in vaccination (e.g., tetanus, cholera, typhoid, plague, anthrax, and tuberculosis), antibiotics, advances in medical diagnostics, lasers, surgical techniques, and routine medicines to treat almost every type of systemic imbalance. Moreover, advances in public health, sanitation, food safety, and geriatric sciences are creating extended life expectancy, where age-related illnesses (osteoarthritis, back pain, neurodegenerative conditions) in addition to NCDs are plaguing an ever-growing elderly population. The age-related risk for these diseases is now worsened by aggregation of global industrial pollutants, where the World Health Organization (WHO) now uses the term “environmental burden ...","internal_url":"https://www.academia.edu/124950476/Epigenetic_Patterns_Therapies_Associated_with_Genetic_Disorders","translated_internal_url":"","created_at":"2024-10-22T08:29:16.203-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Epigenetic_Patterns_Therapies_Associated_with_Genetic_Disorders","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Within the past three centuries, all-cause disease burden in developed countries has shifted from infectious to non-communicable (NCD)/genetic based diseases including cardiovascular conditions, cancer, neuropsychiatric conditions, and diabetes. Factors accounting for this drift include discoveries in vaccination (e.g., tetanus, cholera, typhoid, plague, anthrax, and tuberculosis), antibiotics, advances in medical diagnostics, lasers, surgical techniques, and routine medicines to treat almost every type of systemic imbalance. Moreover, advances in public health, sanitation, food safety, and geriatric sciences are creating extended life expectancy, where age-related illnesses (osteoarthritis, back pain, neurodegenerative conditions) in addition to NCDs are plaguing an ever-growing elderly population. The age-related risk for these diseases is now worsened by aggregation of global industrial pollutants, where the World Health Organization (WHO) now uses the term “environmental burden ...","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":99773,"name":"Disease","url":"https://www.academia.edu/Documents/in/Disease"},{"id":172892,"name":"Life Expectancy","url":"https://www.academia.edu/Documents/in/Life_Expectancy"},{"id":3647879,"name":"Springer Ebooks","url":"https://www.academia.edu/Documents/in/Springer_Ebooks"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950475"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950475/Astrocytic_transcription_factor_REST_upregulates_glutamate_transporter_EAAT2_protecting_dopaminergic_neurons_from_manganese_induced_excitotoxicity"><img alt="Research paper thumbnail of Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity" class="work-thumbnail" src="https://attachments.academia-assets.com/119081014/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950475/Astrocytic_transcription_factor_REST_upregulates_glutamate_transporter_EAAT2_protecting_dopaminergic_neurons_from_manganese_induced_excitotoxicity">Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity</a></div><div class="wp-workCard_item"><span>Journal of Biological Chemistry</span><span>, 2021</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="685f2ab236f63d3c50f2f1ca5543f4a0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081014,"asset_id":124950475,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081014/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950475"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950475"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950475; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "685f2ab236f63d3c50f2f1ca5543f4a0" } } $('.js-work-strip[data-work-id=124950475]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950475,"title":"Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity","translated_title":"","metadata":{"publisher":"Elsevier BV","ai_abstract":"Chronic exposure to manganese (Mn) leads to manganism, resembling Parkinson's disease symptoms, with EAAT2 being crucial for maintaining glutamate levels in the brain. This study identifies that the transcription factor REST enhances EAAT2 expression in astrocytes, thus mitigating Mn-induced excitotoxicity in dopaminergic neurons. REST's mechanism involves recruiting epigenetic modifiers to the EAAT2 promoter, presenting it as a potential target for therapeutic strategies against Mn neurotoxicity and related neurological disorders.","ai_title_tag":"REST Enhances EAAT2 to Protect Neurons from Mn","publication_date":{"day":null,"month":null,"year":2021,"errors":{}},"publication_name":"Journal of Biological Chemistry"},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950475/Astrocytic_transcription_factor_REST_upregulates_glutamate_transporter_EAAT2_protecting_dopaminergic_neurons_from_manganese_induced_excitotoxicity","translated_internal_url":"","created_at":"2024-10-22T08:29:15.959-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081014,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081014/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081014/download_file","bulk_download_file_name":"Astrocytic_transcription_factor_REST_upr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081014/pdf-libre.pdf?1729611329=\u0026response-content-disposition=attachment%3B+filename%3DAstrocytic_transcription_factor_REST_upr.pdf\u0026Expires=1742120023\u0026Signature=Nako0vT2FPCKTTN4KcLD-B9GMHzU2oJGF~1vGaPbkClKTskfDu8yf0Nho58sGst2ddiA~KaLzcnuC2CSAXq~UMNC0AQmid2-u3wGG5HrjqK~ubTkaUZRCKQPWbFrl3D5y56c1yqrKqNU45mWAMZ3u7-7A~1uGRzLyhtDyx5Me2izOuCCrM2KFQTRcKLpYdPUBQ0xw~Ww5eD2B6b5cBRSUC8UBSCZyf4UHLUI9M06ZWYvVm~lNut~HWP5PlL3qQZdTHl9ly2OtbbaSsYOpRShgrWTOlwIDo6XkTMPrPbawVs8Mgc6jR~0ie0o5Gws5SEsMVDXms0qozvUCx2dTBH2rw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Astrocytic_transcription_factor_REST_upregulates_glutamate_transporter_EAAT2_protecting_dopaminergic_neurons_from_manganese_induced_excitotoxicity","translated_slug":"","page_count":16,"language":"en","content_type":"Work","summary":null,"owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081014,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081014/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/119081014/download_file","bulk_download_file_name":"Astrocytic_transcription_factor_REST_upr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081014/pdf-libre.pdf?1729611329=\u0026response-content-disposition=attachment%3B+filename%3DAstrocytic_transcription_factor_REST_upr.pdf\u0026Expires=1742120023\u0026Signature=Nako0vT2FPCKTTN4KcLD-B9GMHzU2oJGF~1vGaPbkClKTskfDu8yf0Nho58sGst2ddiA~KaLzcnuC2CSAXq~UMNC0AQmid2-u3wGG5HrjqK~ubTkaUZRCKQPWbFrl3D5y56c1yqrKqNU45mWAMZ3u7-7A~1uGRzLyhtDyx5Me2izOuCCrM2KFQTRcKLpYdPUBQ0xw~Ww5eD2B6b5cBRSUC8UBSCZyf4UHLUI9M06ZWYvVm~lNut~HWP5PlL3qQZdTHl9ly2OtbbaSsYOpRShgrWTOlwIDo6XkTMPrPbawVs8Mgc6jR~0ie0o5Gws5SEsMVDXms0qozvUCx2dTBH2rw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":18520,"name":"Biological Chemistry","url":"https://www.academia.edu/Documents/in/Biological_Chemistry"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":37851,"name":"Neuroprotection","url":"https://www.academia.edu/Documents/in/Neuroprotection"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":125522,"name":"Neurotoxicity","url":"https://www.academia.edu/Documents/in/Neurotoxicity"},{"id":130116,"name":"Astrocyte","url":"https://www.academia.edu/Documents/in/Astrocyte"},{"id":260118,"name":"CHEMICAL SCIENCES","url":"https://www.academia.edu/Documents/in/CHEMICAL_SCIENCES"},{"id":1151966,"name":"Excitotoxicity","url":"https://www.academia.edu/Documents/in/Excitotoxicity"},{"id":2012816,"name":"Glutamate Receptor","url":"https://www.academia.edu/Documents/in/Glutamate_Receptor"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":45280616,"url":"https://api.elsevier.com/content/article/PII:S0021925821011789?httpAccept=text/xml"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950474"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950474/Molecular_mechanism_of_gossypol_mediating_CCL2_and_IL_8_attenuation_in_triple_negative_breast_cancer_cells"><img alt="Research paper thumbnail of Molecular mechanism of gossypol mediating CCL2 and IL‑8 attenuation in triple‑negative breast cancer cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119081013/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950474/Molecular_mechanism_of_gossypol_mediating_CCL2_and_IL_8_attenuation_in_triple_negative_breast_cancer_cells">Molecular mechanism of gossypol mediating CCL2 and IL‑8 attenuation in triple‑negative breast cancer cells</a></div><div class="wp-workCard_item"><span>Molecular Medicine Reports</span><span>, 2020</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">chronic inflammation associated with cancer is characterized by the production of different types...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">chronic inflammation associated with cancer is characterized by the production of different types of chemokines and cytokines. in cancer, numerous signaling pathways upregulate the expression levels of several cytokines and evolve cells to the neoplastic state. Therefore, targeting these signaling pathways through the inhibition of distinctive gene expression is a primary target for cancer therapy. The present study investigated the anticancer effects of the natural polyphenol gossypol (GoSS) in triple-negative breast cancer (TnBc) cells, the most aggressive breast cancer type with poor prognosis. GoSS effects were examined in two TnBc cell lines: Mda-MB-231 (MM-231) and Mda-MB-468 (MM-468), representing caucasian americans (ca) and african americans (aa), respectively. The obtained ic 50 s revealed no significant difference between the two cell lines' response to the compound. However, the use of microarray assays for cytokine determination indicated the ability of GoSS to attenuate the expression levels of cancer-related cytokines in the two cell lines. although GoSS did not alter ccl2 expression in MM-468 cells, it was able to cause 30% inhibition in TnF-α-stimulated MM-231 cells. additionally, il-8 was not altered by GoSS treatment in MM-231 cells, while its expression was inhibited by 60% in TnF-α-activated MM-468 cells. eliSa assays supported the microarray data and indicated that ccl2 expression was inhibited by 40% in MM-231 cells, and il-8 expression was inhibited by 50% in MM-468 cells. Furthermore, in MM-231 cells, GoSS inhibited ccl2 release via the repression of iKBKe, CCL2 and MAPK1 gene expression. additionally, in MM-468 cells, the compound downregulated the release of il-8 through repressing IL-8, MAPK1, MAPK3, CCDC88A, STAT3 and PIK3CD gene expression. in conclusion, the data obtained in the present study indicate that the polyphenol compound GoSS may provide a valuable tool in TnBc therapy.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3f5507352afdff1e7a4292ff1e8a0d67" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119081013,"asset_id":124950474,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119081013/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950474"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950474"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950474; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950474]").text(description); $(".js-view-count[data-work-id=124950474]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950474; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950474']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "3f5507352afdff1e7a4292ff1e8a0d67" } } $('.js-work-strip[data-work-id=124950474]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950474,"title":"Molecular mechanism of gossypol mediating CCL2 and IL‑8 attenuation in triple‑negative breast cancer cells","translated_title":"","metadata":{"publisher":"Spandidos Publications","ai_title_tag":"Gossypol Reduces CCL2 and IL-8 in Triple-Negative Breast Cancer","grobid_abstract":"chronic inflammation associated with cancer is characterized by the production of different types of chemokines and cytokines. in cancer, numerous signaling pathways upregulate the expression levels of several cytokines and evolve cells to the neoplastic state. Therefore, targeting these signaling pathways through the inhibition of distinctive gene expression is a primary target for cancer therapy. The present study investigated the anticancer effects of the natural polyphenol gossypol (GoSS) in triple-negative breast cancer (TnBc) cells, the most aggressive breast cancer type with poor prognosis. GoSS effects were examined in two TnBc cell lines: Mda-MB-231 (MM-231) and Mda-MB-468 (MM-468), representing caucasian americans (ca) and african americans (aa), respectively. The obtained ic 50 s revealed no significant difference between the two cell lines' response to the compound. However, the use of microarray assays for cytokine determination indicated the ability of GoSS to attenuate the expression levels of cancer-related cytokines in the two cell lines. although GoSS did not alter ccl2 expression in MM-468 cells, it was able to cause 30% inhibition in TnF-α-stimulated MM-231 cells. additionally, il-8 was not altered by GoSS treatment in MM-231 cells, while its expression was inhibited by 60% in TnF-α-activated MM-468 cells. eliSa assays supported the microarray data and indicated that ccl2 expression was inhibited by 40% in MM-231 cells, and il-8 expression was inhibited by 50% in MM-468 cells. Furthermore, in MM-231 cells, GoSS inhibited ccl2 release via the repression of iKBKe, CCL2 and MAPK1 gene expression. additionally, in MM-468 cells, the compound downregulated the release of il-8 through repressing IL-8, MAPK1, MAPK3, CCDC88A, STAT3 and PIK3CD gene expression. in conclusion, the data obtained in the present study indicate that the polyphenol compound GoSS may provide a valuable tool in TnBc therapy.","publication_date":{"day":null,"month":null,"year":2020,"errors":{}},"publication_name":"Molecular Medicine Reports","grobid_abstract_attachment_id":119081013},"translated_abstract":null,"internal_url":"https://www.academia.edu/124950474/Molecular_mechanism_of_gossypol_mediating_CCL2_and_IL_8_attenuation_in_triple_negative_breast_cancer_cells","translated_internal_url":"","created_at":"2024-10-22T08:29:15.771-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":7953118,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119081013,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081013/thumbnails/1.jpg","file_name":"download.pdf","download_url":"https://www.academia.edu/attachments/119081013/download_file","bulk_download_file_name":"Molecular_mechanism_of_gossypol_mediatin.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081013/download-libre.pdf?1729611338=\u0026response-content-disposition=attachment%3B+filename%3DMolecular_mechanism_of_gossypol_mediatin.pdf\u0026Expires=1742120023\u0026Signature=WM8rDvL9U05zJALk6Kb0M2EGa5D4LmsUQcmNgTCvUs-LvMAumFhmyej59pz1YuxTn~AAytKKZesz3i-Tuha3yLK~z6iFuPGjRtb~t7wsot8AQTnVViP07NnozifGIdkxd-Nb-Q0TZcHAroNYitsFsm84I5jLTD0s1wqcb-4ptr9EPClu169dK1~Zao7yFJNaRvhIIL9DqGRD89nlwEohsMuDht6lNXxw-pYy33S3m~D3WC5KluWHloh0GF7GzcxYe5OE2jXwilunrJB96gOwhNa600kK2ZsIoyHk9~YlnFnozq81dov7JoEkqYemrqOTMJXBiFTmMA2lHzKOvJEoSw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Molecular_mechanism_of_gossypol_mediating_CCL2_and_IL_8_attenuation_in_triple_negative_breast_cancer_cells","translated_slug":"","page_count":14,"language":"en","content_type":"Work","summary":"chronic inflammation associated with cancer is characterized by the production of different types of chemokines and cytokines. in cancer, numerous signaling pathways upregulate the expression levels of several cytokines and evolve cells to the neoplastic state. Therefore, targeting these signaling pathways through the inhibition of distinctive gene expression is a primary target for cancer therapy. The present study investigated the anticancer effects of the natural polyphenol gossypol (GoSS) in triple-negative breast cancer (TnBc) cells, the most aggressive breast cancer type with poor prognosis. GoSS effects were examined in two TnBc cell lines: Mda-MB-231 (MM-231) and Mda-MB-468 (MM-468), representing caucasian americans (ca) and african americans (aa), respectively. The obtained ic 50 s revealed no significant difference between the two cell lines' response to the compound. However, the use of microarray assays for cytokine determination indicated the ability of GoSS to attenuate the expression levels of cancer-related cytokines in the two cell lines. although GoSS did not alter ccl2 expression in MM-468 cells, it was able to cause 30% inhibition in TnF-α-stimulated MM-231 cells. additionally, il-8 was not altered by GoSS treatment in MM-231 cells, while its expression was inhibited by 60% in TnF-α-activated MM-468 cells. eliSa assays supported the microarray data and indicated that ccl2 expression was inhibited by 40% in MM-231 cells, and il-8 expression was inhibited by 50% in MM-468 cells. Furthermore, in MM-231 cells, GoSS inhibited ccl2 release via the repression of iKBKe, CCL2 and MAPK1 gene expression. additionally, in MM-468 cells, the compound downregulated the release of il-8 through repressing IL-8, MAPK1, MAPK3, CCDC88A, STAT3 and PIK3CD gene expression. in conclusion, the data obtained in the present study indicate that the polyphenol compound GoSS may provide a valuable tool in TnBc therapy.","owner":{"id":7953118,"first_name":"Karam","middle_initials":null,"last_name":"Soliman","page_name":"KSoliman","domain_name":"famu","created_at":"2014-01-02T02:06:45.180-08:00","display_name":"Karam Soliman","url":"https://famu.academia.edu/KSoliman"},"attachments":[{"id":119081013,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119081013/thumbnails/1.jpg","file_name":"download.pdf","download_url":"https://www.academia.edu/attachments/119081013/download_file","bulk_download_file_name":"Molecular_mechanism_of_gossypol_mediatin.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119081013/download-libre.pdf?1729611338=\u0026response-content-disposition=attachment%3B+filename%3DMolecular_mechanism_of_gossypol_mediatin.pdf\u0026Expires=1742120023\u0026Signature=WM8rDvL9U05zJALk6Kb0M2EGa5D4LmsUQcmNgTCvUs-LvMAumFhmyej59pz1YuxTn~AAytKKZesz3i-Tuha3yLK~z6iFuPGjRtb~t7wsot8AQTnVViP07NnozifGIdkxd-Nb-Q0TZcHAroNYitsFsm84I5jLTD0s1wqcb-4ptr9EPClu169dK1~Zao7yFJNaRvhIIL9DqGRD89nlwEohsMuDht6lNXxw-pYy33S3m~D3WC5KluWHloh0GF7GzcxYe5OE2jXwilunrJB96gOwhNa600kK2ZsIoyHk9~YlnFnozq81dov7JoEkqYemrqOTMJXBiFTmMA2lHzKOvJEoSw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":6021,"name":"Cancer","url":"https://www.academia.edu/Documents/in/Cancer"},{"id":22255,"name":"Cancer Research","url":"https://www.academia.edu/Documents/in/Cancer_Research"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":106169,"name":"Oncogene","url":"https://www.academia.edu/Documents/in/Oncogene"},{"id":291150,"name":"Triple Negative Breast Cancer","url":"https://www.academia.edu/Documents/in/Triple_Negative_Breast_Cancer"},{"id":1461942,"name":"CCL","url":"https://www.academia.edu/Documents/in/CCL"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950473"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950473/Identification_of_cytotoxic_markers_in_methamphetamine_treated_rat_C6_astroglia_like_cells"><img alt="Research paper thumbnail of Identification of cytotoxic markers in methamphetamine treated rat C6 astroglia-like cells" class="work-thumbnail" src="https://attachments.academia-assets.com/119080987/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950473/Identification_of_cytotoxic_markers_in_methamphetamine_treated_rat_C6_astroglia_like_cells">Identification of cytotoxic markers in methamphetamine treated rat C6 astroglia-like cells</a></div><div class="wp-workCard_item"><span>Scientific Reports</span><span>, 2019</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Methamphetamine (METH) is a powerfully addictive psychostimulant that has a pronounced effect on ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Methamphetamine (METH) is a powerfully addictive psychostimulant that has a pronounced effect on the central nervous system (CNS). The present study aimed to assess METH toxicity in differentiated C6 astroglia-like cells through biochemical and toxicity markers with acute (1 h) and chronic (48 h) treatments. In the absence of external stimulants, cellular differentiation of neuronal morphology was achieved through reduced serum (2.5%) in the medium. The cells displayed branched neurite-like processes with extensive intercellular connections. Results indicated that acute METH treatment neither altered the cell morphology nor killed the cells, which echoed with lack of consequence on reactive oxygen species (ROS), nitric oxide (NO) or inhibition of any cell cycle phases except induction of cytoplasmic vacuoles. On the other hand, chronic treatment at 1 mM or above destroyed the neurite-like processors and decreased the cell viability that paralleled with increased levels of ROS, lipid...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0586728ee04773ae3a42bf0be79bac62" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119080987,"asset_id":124950473,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119080987/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950473"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950473"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950473; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950473]").text(description); $(".js-view-count[data-work-id=124950473]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950473; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950473']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0586728ee04773ae3a42bf0be79bac62" } } $('.js-work-strip[data-work-id=124950473]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950473,"title":"Identification of cytotoxic markers in methamphetamine treated rat C6 astroglia-like cells","translated_title":"","metadata":{"abstract":"Methamphetamine (METH) is a powerfully addictive psychostimulant that has a pronounced effect on the central nervous system (CNS). 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="124950472"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/124950472/The_Research_Centers_in_Minority_Institutions_RCMI_Translational_Research_Network_Building_and_Sustaining_Capacity_for_Multi_Site_Basic_Biomedical_Clinical_and_Behavioral_Research"><img alt="Research paper thumbnail of The Research Centers in Minority Institutions (RCMI) Translational Research Network: Building and Sustaining Capacity for Multi-Site Basic Biomedical, Clinical and Behavioral Research" class="work-thumbnail" src="https://attachments.academia-assets.com/119080986/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/124950472/The_Research_Centers_in_Minority_Institutions_RCMI_Translational_Research_Network_Building_and_Sustaining_Capacity_for_Multi_Site_Basic_Biomedical_Clinical_and_Behavioral_Research">The Research Centers in Minority Institutions (RCMI) Translational Research Network: Building and Sustaining Capacity for Multi-Site Basic Biomedical, Clinical and Behavioral Research</a></div><div class="wp-workCard_item"><span>Ethnicity & Disease</span><span>, 2019</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The Research Centers in Minority Institutions (RCMI) program was established by the US Congress ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The Research Centers in Minority Institutions (RCMI) program was established by the US Congress to support the development of biomedical research infrastructure at minority-serving institutions granting doctoral degrees in the health professions or in a health-related science. RCMI institutions also conduct research on diseases that disproportionately affect racial and ethnic minorities (ie, African Americans/Blacks, American Indians and Alaska Natives, Hispanics, Native Hawaiians and Other Pacific Islanders), those of low socioeconomic status, and rural persons. Quantitative metrics, including the numbers of doctoral science degrees granted to underrepresented students, NIH peer-reviewed research funding, peer-reviewed publications, and numbers of racial and ethnic minorities participating in sponsored research, demonstrate that RCMI grantee institutions have made substantial progress toward the intent of the Congressional legislation, as well as the NIH/NIMHD-linked goals o...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="dbd852d1096129bdb6d53184736dba0a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119080986,"asset_id":124950472,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119080986/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="124950472"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="124950472"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 124950472; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=124950472]").text(description); $(".js-view-count[data-work-id=124950472]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 124950472; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='124950472']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "dbd852d1096129bdb6d53184736dba0a" } } $('.js-work-strip[data-work-id=124950472]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":124950472,"title":"The Research Centers in Minority Institutions (RCMI) Translational Research Network: Building and Sustaining Capacity for Multi-Site Basic Biomedical, Clinical and Behavioral Research","translated_title":"","metadata":{"abstract":"The Research Centers in Minority Institutions (RCMI) program was established by the US Congress to support the development of biomedical research infrastructure at minority-serving institutions granting doctoral degrees in the health professions or in a health-related science. 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