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migration assays</title> <meta name="description" content="Search results for: cell migration assays"> <meta name="keywords" content="cell migration assays"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button class="d-block 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action="https://publications.waset.org/abstracts/search"> <div id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="cell migration assays"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 4848</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: cell migration assays</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4848</span> Influence of Preheating Self-Adhesive Cements on the Degree of Conversion, Cell Migration and Cell Viability in NIH/3T3</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Celso%20Afonso%20Klein%20Jr.">Celso Afonso Klein Jr.</a>, <a href="https://publications.waset.org/abstracts/search?q=Henrique%20Cantarelli"> Henrique Cantarelli</a>, <a href="https://publications.waset.org/abstracts/search?q=Fernando%20Portella"> Fernando Portella</a>, <a href="https://publications.waset.org/abstracts/search?q=Keiichi%20Hosaka"> Keiichi Hosaka</a>, <a href="https://publications.waset.org/abstracts/search?q=Eduardo%20Reston"> Eduardo Reston</a>, <a href="https://publications.waset.org/abstracts/search?q=Fabricio%20Collares"> Fabricio Collares</a>, <a href="https://publications.waset.org/abstracts/search?q=Roberto%20Zimmer"> Roberto Zimmer</a> </p> <p class="card-text"><strong>Abstract:</strong></p> TTo evaluate the influence of preheating self-adhesive cement at 39ºC on cell migration, cytotoxicity and degree of conversion. RelyX U200, Set PP and MaxCem Elite were subjected to a degree of conversion analysis (FTIR-ATR). For the cytotoxicity analysis, extracts (24 h and 7 days) were placed in contact with NIH/3T3 cells. For cell migration, images were captured of each sample until the possible closure of the cleft occurred. In the results of the degree of conversion, preheating did not improve the conversion of cement. For the MTT, preheating did not improve the results within 24 hours. However, it generated positive results within 7 days for the Set PP resin cement. For cell migration, high rates of cell death were found in all groups. It is concluded that preheating at 39ºC caused a positive effect only in increasing the cell viability of the Set PP resin cement and that both materials analyzed are highly cytotoxic. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=dental%20cements" title="dental cements">dental cements</a>, <a href="https://publications.waset.org/abstracts/search?q=resin%20cements" title=" resin cements"> resin cements</a>, <a href="https://publications.waset.org/abstracts/search?q=degree%20of%20conversion" title=" degree of conversion"> degree of conversion</a>, <a href="https://publications.waset.org/abstracts/search?q=cytotoxicity" title=" cytotoxicity"> cytotoxicity</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20migration%20assays" title=" cell migration assays"> cell migration assays</a> </p> <a href="https://publications.waset.org/abstracts/179105/influence-of-preheating-self-adhesive-cements-on-the-degree-of-conversion-cell-migration-and-cell-viability-in-nih3t3" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/179105.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">72</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4847</span> DSC2 Promotes the Proliferation, Metastasis and Drug Resistance of Lung Cancer by Activating the PI3K/AKT Pathway</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Qi%20LI">Qi LI</a>, <a href="https://publications.waset.org/abstracts/search?q=Xu%20Lin"> Xu Lin</a>, <a href="https://publications.waset.org/abstracts/search?q=Nengming%20Lin"> Nengming Lin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objective: The aim of this study was to investigate the role of desmocollin 2 (DSC2) protein in the proliferation, migration and drug resistance of lung cancer cells. Method: CCK-8 assays and colony formation assays were used to evaluate the effect of dsc2 regulation on cancer cell viability and colony formation. Transwell assays and wound healing assays were also performed. Cell flow double staining was used to detect the apoptosis rate of cells with DSC2, which was added cisplatin. Western blot assay was used to detect cell cycle, PI3k/Akt and apoptosis-related proteins. Results: Our data showed that dsc2 is upregulated in clinical lung cancer tissues compared with pericarcinomatous tissues, and it is differentially expressed in lung cancer cell lines. The down-regulation of dsc2 in A549 and H358 lung cancer cells significantly suppressed the cell proliferation, metastasis, and motility. In contrast, the opposite effects were observed in overexpression of dsc2 both in H23 and PC9 cell lines. In addition to lung adenocarcinoma cell lines, we also examined its expression in lung squamous cell lines, such as H226. Western blotting showed that dsc2 could reduce the level of phosphorylated Akt (Ser 473) and p-mTOR. Thus, it is speculated that dsc2 up-regulation promotes proliferation and invasiveness through activation of the PI3K/AKT pathway. Also, knockdown of dsc2 in A549 and H226 could significantly decreased in the levels of cyclinB and wee1 protein. Additionally, flow cytometry showed that dsc2 knockdown combined with cisplatin could significantly enhance cell apoptosis rate. Conclusion: These data suggest that dsc2 promotes the proliferation and migration of lung cancer cells in vitro. Also, the results suggested that dsc2 could affect the cell cycle and apoptosis of lung cells. Furthermore, knockdown of dsc2 could sensitize cisplatin in both lung adenocarcinoma and lung squamous cell lines. Thus we suggested that dsc2 can be used as a therapeutic target for lung cancer. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=desmocollin%202" title="desmocollin 2">desmocollin 2</a>, <a href="https://publications.waset.org/abstracts/search?q=cisplatin" title=" cisplatin"> cisplatin</a>, <a href="https://publications.waset.org/abstracts/search?q=lung%20cancer" title=" lung cancer"> lung cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=PI3K%2FAKT" title=" PI3K/AKT"> PI3K/AKT</a>, <a href="https://publications.waset.org/abstracts/search?q=lung%20squamous%20cell" title=" lung squamous cell"> lung squamous cell</a> </p> <a href="https://publications.waset.org/abstracts/167679/dsc2-promotes-the-proliferation-metastasis-and-drug-resistance-of-lung-cancer-by-activating-the-pi3kakt-pathway" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/167679.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">76</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4846</span> Fam111b Gene Dysregulation Contributes to the Malignancy in Fibrosarcoma, Poor Clinical Outcomes in Poiktmp and a Low-cost Method for Its Mutation Screening</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Cenza%20Rhoda">Cenza Rhoda</a>, <a href="https://publications.waset.org/abstracts/search?q=Falone%20Sunda"> Falone Sunda</a>, <a href="https://publications.waset.org/abstracts/search?q=Elvis%20Kidzeru"> Elvis Kidzeru</a>, <a href="https://publications.waset.org/abstracts/search?q=Nonhlanhla%20P.%20Khumalo"> Nonhlanhla P. Khumalo</a>, <a href="https://publications.waset.org/abstracts/search?q=Afolake%20Arowolo"> Afolake Arowolo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: The human FAM111B gene mutations are associated with POIKTMP, a rare multi-organ fibrosing disease. Recent studies also reported the overexpression of FAM111B in specific cancers. However, the role of FAM111B in these pathologies, particularly fibrosarcoma, remains unknown. Materials and Methods: FAM111B RNA expression in some cancer cell lines was assessed in silico and validated in vitro in these cell lines and skin fibroblasts derived from the South African family member affected by POIKTMP with the heterozygous FAM111B gene mutation: NM_198947.4: c.1861T>G (p. Tyr621Asp or Y621D) by qPCR and western blot. The cellular function of FAM111B was also studied in HT1080 using various cell-based functional assays and a simple and cost-effective PCR-RFLP method for genotyping/screening FAM111B gene mutations described. Results: Expression studies showed upregulated FAM111B mRNA and protein in the cancer cells. High FAM111B expression with robust nuclear localization occurred in HT1080. Additionally, expression data and cell-based assays indicated that FAM111B led to the upregulation of cell migration and decreased cell apoptosis and cell proliferation modulation. FAM111B Y621D mutation showed similar effects on cell migration but minimal impact on cell apoptosis. FAM111B mRNA and protein expression were markedly downregulated (p ≤ 0.05) in the patient's skin-derived fibroblasts. Lastly, the PCR-RFLP method successfully genotyped FAM111B Y621D gene mutation. Discussion: FAM111B is a cancer-associated nuclear protein: Its modulation by mutations may enhance cell migration and proliferation and decrease apoptosis, as seen in cancers and POIKTMP/fibrosis, thus representing a viable therapeutic target in these disorders. Furthermore, the PCR-RFLP method could prove a valuable tool for FAM111B mutation validation or screening in resource-constrained laboratories. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=FAM111B" title="FAM111B">FAM111B</a>, <a href="https://publications.waset.org/abstracts/search?q=POIKTMP" title=" POIKTMP"> POIKTMP</a>, <a href="https://publications.waset.org/abstracts/search?q=cancer" title=" cancer"> cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=PCR-RFLP" title=" PCR-RFLP"> PCR-RFLP</a> </p> <a href="https://publications.waset.org/abstracts/159155/fam111b-gene-dysregulation-contributes-to-the-malignancy-in-fibrosarcoma-poor-clinical-outcomes-in-poiktmp-and-a-low-cost-method-for-its-mutation-screening" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/159155.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">121</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4845</span> Novel Aminoglycosides to Target Resistant Pathogens</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Nihar%20Ranjan">Nihar Ranjan</a>, <a href="https://publications.waset.org/abstracts/search?q=Derrick%20Watkins"> Derrick Watkins</a>, <a href="https://publications.waset.org/abstracts/search?q=Dev%20P.%20Arya"> Dev P. Arya</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Current methods in the study of antibiotic activity of ribosome targeted antibiotics are dependent on cell based bacterial inhibition assays or various forms of ribosomal binding assays. These assays are typically independent of each other and little direct correlation between the ribosomal binding and bacterial inhibition is established with the complementary assay. We have developed novel high-throughput capable assays for ribosome targeted drug discovery. One such assay examines the compounds ability to bind to a model ribosomal RNA A-site. We have also coupled this assay to other functional orthogonal assays. Such analysis can provide valuable understanding of the relationships between two complementary drug screening methods and could be used as standard analysis to correlate the affinity of a compound for its target and the effect the compound has on a cell. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bacterial%20resistance" title="bacterial resistance">bacterial resistance</a>, <a href="https://publications.waset.org/abstracts/search?q=aminoglycosides" title=" aminoglycosides"> aminoglycosides</a>, <a href="https://publications.waset.org/abstracts/search?q=screening" title=" screening"> screening</a>, <a href="https://publications.waset.org/abstracts/search?q=drugs" title=" drugs"> drugs</a> </p> <a href="https://publications.waset.org/abstracts/16341/novel-aminoglycosides-to-target-resistant-pathogens" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/16341.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">370</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4844</span> Dual Drug Piperine-Paclitaxel Nanoparticles Inhibit Migration and Invasion in Human Breast Cancer Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Monika%20Verma">Monika Verma</a>, <a href="https://publications.waset.org/abstracts/search?q=Renuka%20Sharma"> Renuka Sharma</a>, <a href="https://publications.waset.org/abstracts/search?q=B.%20R.%20Gulati"> B. R. Gulati</a>, <a href="https://publications.waset.org/abstracts/search?q=Namita%20Singh"> Namita Singh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In combination therapy, two chemotherapeutic agents work together in a collaborative action. It has appeared as one of the promising approaches to improve anti-cancer treatment efficacy. In the present investigation, piperine (P-NPS), paclitaxel (PTX NPS), and a combination of both, piperine-paclitaxel nanoparticle (Pip-PTX NPS), were made by the nanoprecipitation method and later characterized by PSA, DSC, SEM, TEM, and FTIR. All nanoparticles exhibited a monodispersed size distribution with a size of below 200 nm, zeta potential ranges from (-30-40mV) and a narrow polydispersity index (>0.3) of the drugs. The average encapsulation efficiency was found to be between 80 and 90%. In vitro release of drugs for nanoparticles was done spectrophotometrically. FTIR and DSC results confirmed the presence of the drug. The Pip-PTX NPS significantly inhibit cell proliferation as compared to the native drugs nanoparticles in the breast cancer cell line MCF-7. In addition, Pip-PTX NPS suppresses cells in colony formation and soft gel agar assay. Scratch migration and Transwell chamber invasion assays revealed that combined nanoparticles reduce the migration and invasion of breast cancer cells. Morphological studies showed that Pip-PTX NPS penetrates the cells and induces apoptosis, which was further confirmed by DNA fragmentation, SEM, and western blot analysis. Taken together, Pip-PTX NPS inhibits cell proliferation, anchorage dependent and anchorage independent cell growth, reduces migration and invasion, and induces apoptosis in cells. These findings support that combination therapy using Pip-PTX NPS represents a potential approach and could be helpful in the future for breast cancer therapy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=piperine" title="piperine">piperine</a>, <a href="https://publications.waset.org/abstracts/search?q=paclitaxel" title=" paclitaxel"> paclitaxel</a>, <a href="https://publications.waset.org/abstracts/search?q=breast%20cancer" title=" breast cancer"> breast cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title=" apoptosis"> apoptosis</a> </p> <a href="https://publications.waset.org/abstracts/154025/dual-drug-piperine-paclitaxel-nanoparticles-inhibit-migration-and-invasion-in-human-breast-cancer-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/154025.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">101</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4843</span> Study of the Combinatorial Impact of Substrate Properties on Mesenchymal Stem Cell Migration Using Microfluidics</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Nishanth%20Venugopal%20Menon">Nishanth Venugopal Menon</a>, <a href="https://publications.waset.org/abstracts/search?q=Chuah%20Yon%20Jin"> Chuah Yon Jin</a>, <a href="https://publications.waset.org/abstracts/search?q=Samantha%20Phey"> Samantha Phey</a>, <a href="https://publications.waset.org/abstracts/search?q=Wu%20Yingnan"> Wu Yingnan</a>, <a href="https://publications.waset.org/abstracts/search?q=Zhang%20Ying"> Zhang Ying</a>, <a href="https://publications.waset.org/abstracts/search?q=Vincent%20Chan"> Vincent Chan</a>, <a href="https://publications.waset.org/abstracts/search?q=Kang%20Yuejun"> Kang Yuejun</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Cell Migration is a vital phenomenon that the cells undergo in various physiological processes like wound healing, disease progression, embryogenesis, etc. Cell migration depends primarily on the chemical and physical cues available in the cellular environment. The chemical cue involves the chemokines secreted and gradients generated in the environment while physical cues indicate the impact of matrix properties like nanotopography and stiffness on the cells. Mesenchymal Stem Cells (MSCs) have been shown to have a role wound healing in vivo and its migration to the site of the wound has been shown to have a therapeutic effect. In the field of stem cell based tissue regeneration of bones and cartilage, one approach has been to introduce scaffold laden with MSCs into the site of injury to enable tissue regeneration. In this work, we have studied the combinatorial impact of the substrate physical properties on MSC migration. A microfluidic in vitro model was created to perform the migration studies. The microfluidic model used is a three compartment device consisting of two cell seeding compartments and one migration compartment. Four different PDMS substrates with varying substrate roughness, stiffness and hydrophobicity were created. Its surface roughness and stiffness was measured using Atomic Force Microscopy (AFM) while its hydrphobicity was measured from the water contact angle using an optical tensiometer. These PDMS substrates are sealed to the microfluidic chip following which the MSCs are seeded and the cell migration is studied over the period of a week. Cell migration was quantified using fluorescence imaging of the cytoskeleton (F-actin) to find out the area covered by the cells inside the migration compartment. The impact of adhesion proteins on cell migration was also quantified using a real-time polymerase chain reaction (qRT PCR). These results suggested that the optimal substrate for cell migration would be one with an intermediate level of roughness, stiffness and hydrophobicity. A higher or lower value of these properties affected cell migration negatively. These observations have helped us in understanding that different substrate properties need to be considered in tandem, especially while designing scaffolds for tissue regeneration as cell migration is normally impacted by the combinatorial impact of the matrix. These observations may lead us to scaffold optimization in future tissue regeneration applications. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cell%20migration" title="cell migration">cell migration</a>, <a href="https://publications.waset.org/abstracts/search?q=microfluidics" title=" microfluidics"> microfluidics</a>, <a href="https://publications.waset.org/abstracts/search?q=in%20vitro%20model" title=" in vitro model"> in vitro model</a>, <a href="https://publications.waset.org/abstracts/search?q=stem%20cell%20migration" title=" stem cell migration"> stem cell migration</a>, <a href="https://publications.waset.org/abstracts/search?q=scaffold" title=" scaffold"> scaffold</a>, <a href="https://publications.waset.org/abstracts/search?q=substrate%20properties" title=" substrate properties"> substrate properties</a> </p> <a href="https://publications.waset.org/abstracts/26874/study-of-the-combinatorial-impact-of-substrate-properties-on-mesenchymal-stem-cell-migration-using-microfluidics" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/26874.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">557</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4842</span> The Biological Function and Clinical Significance of Long Non-coding RNA LINC AC008063 in Head and Neck Squamous Carcinoma</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Maierhaba%20Mijiti">Maierhaba Mijiti</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objective：The aim is to understand the relationship between the expression level of the long-non-coding RNA LINC AC008063 and the clinicopathological parameters of patients with head and neck squamous cell carcinoma (HNSCC), and to clarify the biological function of LINC AC008063 in HNSCC cells. Moreover, it provides a potential biomarker for the diagnosis, treatment, and prognosis evaluation of HNSCC. Methods: The expression level of LINC AC008063 in the HNSCC was analyzed using transcriptome sequencing data from the TCGA (The cancer genome atlas) database. The expression levels of LINC AC008063 in human embryonic lung diploid cells 2BS, human immortalized keratinocytes HACAT, HNSCC cell lines CAL-27, Detroit562, AMC-HN-8, FD-LSC-1, FaDu and WSU-HN30 were determined by real-time quantitative PCR (qPCR). RNAi (RNA interference) was introduced for LINC AC008063 knockdown in HNSCC cell lines, the localization and abundance analysis of LINC AC008063 was determined by RT-qPCR, and the biological functions were examined by CCK-8, clone formation, flow cytometry, transwell invasion and migration assays, Seahorse assay. Results: LINC AC008063 was upregulated in HNSCC tissue (P<0.001), and verified b CCK-8, clone formation, flow cytometry, transwell invasion and migration assays, Seahorse assayy qPCR in HNSCC cell lines. The survival analysis revealed that the overall survival rate (OS) of patients with high LINC AC008063 expression group was significantly lower than that in the LINC AC008063 expression group, the median survival times for the two groups were 33.10 months and 61.27 months, respectively (P=0.002). The clinical correlation analysis revealed that its expression was positively correlated with the age of patients with HNSCC (P<0.001) and positively correlated with pathological state (T3+T4＞T1+T2, P=0.03). The RT-qPCR results showed that LINC AC008063 was mainly enriched in cytoplasm (P=0.01). Knockdown of LINC AC008063 inhibited proliferation, colony formation, migration and invasion; the glycolytic capacity was significantly decreased in HNSCC cell lines (P＜0.05). Conclusion: High level of LINC AC008063 was associated with the malignant progression of HNSCC as well as promoting the important biological functions of proliferation, colony formation, migration and invasion; in particular, the glycolytic capacity was decreased in HNSCC cells. Therefore, LINC AC008063 may serve as a potential biomarker for HNSCC and a distinct molecular target to inhibit glycolysis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=head%20and%20neck%20squamous%20cell%20carcinoma" title="head and neck squamous cell carcinoma">head and neck squamous cell carcinoma</a>, <a href="https://publications.waset.org/abstracts/search?q=oncogene" title=" oncogene"> oncogene</a>, <a href="https://publications.waset.org/abstracts/search?q=long%20non-coding%20RNA" title=" long non-coding RNA"> long non-coding RNA</a>, <a href="https://publications.waset.org/abstracts/search?q=LINC%20AC008063" title=" LINC AC008063"> LINC AC008063</a>, <a href="https://publications.waset.org/abstracts/search?q=invasion%20and%20metastasis" title=" invasion and metastasis"> invasion and metastasis</a> </p> <a href="https://publications.waset.org/abstracts/194321/the-biological-function-and-clinical-significance-of-long-non-coding-rna-linc-ac008063-in-head-and-neck-squamous-carcinoma" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/194321.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">10</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4841</span> Numerical Simulation of a Single Cell Passing through a Narrow Slit</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Lanlan%20Xiao">Lanlan Xiao</a>, <a href="https://publications.waset.org/abstracts/search?q=Yang%20Liu"> Yang Liu</a>, <a href="https://publications.waset.org/abstracts/search?q=Shuo%20Chen"> Shuo Chen</a>, <a href="https://publications.waset.org/abstracts/search?q=Bingmei%20Fu"> Bingmei Fu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Most cancer-related deaths are due to metastasis. Metastasis is a complex, multistep processes including the detachment of cancer cells from the primary tumor and the migration to distant targeted organs through blood and/or lymphatic circulations. During hematogenous metastasis, the emigration of tumor cells from the blood stream through the vascular wall into the tissue involves arrest in the microvasculature, adhesion to the endothelial cells forming the microvessel wall and transmigration to the tissue through the endothelial barrier termed as extravasation. The narrow slit between endothelial cells that line the microvessel wall is the principal pathway for tumor cell extravasation to the surrounding tissue. To understand this crucial step for tumor hematogenous metastasis, we used Dissipative Particle Dynamics method to investigate an individual cell passing through a narrow slit numerically. The cell membrane was simulated by a spring-based network model which can separate the internal cytoplasm and surrounding fluid. The effects of the cell elasticity, cell shape and cell surface area increase, and slit size on the cell transmigration through the slit were investigated. Under a fixed driven force, the cell with higher elasticity can be elongated more and pass faster through the slit. When the slit width decreases to 2/3 of the cell diameter, the spherical cell becomes jammed despite reducing its elasticity modulus by 10 times. However, transforming the cell from a spherical to ellipsoidal shape and increasing the cell surface area only by 3% can enable the cell to pass the narrow slit. Therefore the cell shape and surface area increase play a more important role than the cell elasticity in cell passing through the narrow slit. In addition, the simulation results indicate that the cell migration velocity decreases during entry but increases during exit of the slit, which is qualitatively in agreement with the experimental observation. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=dissipative%20particle%20dynamics" title="dissipative particle dynamics">dissipative particle dynamics</a>, <a href="https://publications.waset.org/abstracts/search?q=deformability" title=" deformability"> deformability</a>, <a href="https://publications.waset.org/abstracts/search?q=surface%20area%20increase" title=" surface area increase"> surface area increase</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20migration" title=" cell migration"> cell migration</a> </p> <a href="https://publications.waset.org/abstracts/40189/numerical-simulation-of-a-single-cell-passing-through-a-narrow-slit" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/40189.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">334</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4840</span> A Fluid-Walled Microfluidic Device for Cell Migration Studies</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Cyril%20Deroy">Cyril Deroy</a>, <a href="https://publications.waset.org/abstracts/search?q=Agata%20Rumianek"> Agata Rumianek</a>, <a href="https://publications.waset.org/abstracts/search?q=David%20R.%20Greaves"> David R. Greaves</a>, <a href="https://publications.waset.org/abstracts/search?q=Peter%20R.%20Cook"> Peter R. Cook</a>, <a href="https://publications.waset.org/abstracts/search?q=Edmond%20J.%20Walsh"> Edmond J. Walsh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Various microfluidic platforms have been developed in the past couple of decades offering experimental methods for the study of cell migration; however, their implementation in the laboratory has remained limited. Some reasons cited for the lack of uptake include the technical complexity of the devices, high failure rate associated with gas-bubbles, biocompatibility concerns with the use of polydimethylsiloxane (PDMS) and equipment/time/expertise requirements for operation and manufacture. As sample handling remains challenging due to the closed format of microfluidic devices, open microfluidic systems have been developed offering versatility and simplicity of use. Rather than confining fluids by solid walls, samples can be accessed directly over the open platform, by removing at least one of the solid boundaries, such as the cover. In this paper, a method for the fabrication of open fluid-walled microfluidic circuits for cell migration studies is introduced, where only materials commonly used by the life-science community are required; tissue culture dishes and cell media. The simplicity of the method, and ability to retrieve cells of interest are two key features of the method. Both passive and active flow-devices can be created in this way. To demonstrate the versatility of the method a cell migration assay is performed, which requires fabricating circuits for establishing chemical gradients, loading cells and incubating, creating chemical gradients, real time imaging of cell migration and finally retrieval of cells. The open architecture has high fidelity as it eliminates air bubble related failures and enables the precise control of gradients. The ability to fabricate custom microfluidic designs in minutes should make this method suitable for use in a wide range of cell migration studies. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=chemotaxis" title="chemotaxis">chemotaxis</a>, <a href="https://publications.waset.org/abstracts/search?q=fluid%20walls" title=" fluid walls"> fluid walls</a>, <a href="https://publications.waset.org/abstracts/search?q=gradient%20generation" title=" gradient generation"> gradient generation</a>, <a href="https://publications.waset.org/abstracts/search?q=open%20microfluidics" title=" open microfluidics"> open microfluidics</a> </p> <a href="https://publications.waset.org/abstracts/100370/a-fluid-walled-microfluidic-device-for-cell-migration-studies" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/100370.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">149</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4839</span> Non-Signaling Chemokine Receptor CCRL1 and Its Active Counterpart CCR7 in Prostate Cancer</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yiding%20Qu">Yiding Qu</a>, <a href="https://publications.waset.org/abstracts/search?q=Svetlana%20V.%20Komarova"> Svetlana V. Komarova</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Chemokines acting through their cognate chemokine receptors guide the directional migration of the cell along the chemokine gradient. Several chemokine receptors were recently identified as non-signaling (decoy), based on their ability to bind the chemokine but produce no measurable signal in the cell. The function of these decoy receptors is not well understood. We examined the expression of a decoy receptor CCRL1 and a signaling receptor that binds to the same ligands, CCR7, in prostate cancer using publically available microarray data (www.oncomine.org). The expression of both CCRL1 and CCR7 increased in an approximately half of prostate carcinoma samples and the majority of metastatic cancer samples compared to normal prostate. Moreover, the expression of CCRL1 positively correlated with the expression of CCR7. These data suggest that CCR7 and CCRL1 can be used as clinical markers for the early detection of transformation from carcinoma to metastatic cancer. In addition, these data support our hypothesis that the non-signaling chemokine receptors actively stimulate cell migration. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bioinformatics" title="bioinformatics">bioinformatics</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20migration" title=" cell migration"> cell migration</a>, <a href="https://publications.waset.org/abstracts/search?q=decoy%20receptor" title=" decoy receptor"> decoy receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=meta-analysis" title=" meta-analysis"> meta-analysis</a>, <a href="https://publications.waset.org/abstracts/search?q=prostate%20cancer" title=" prostate cancer"> prostate cancer</a> </p> <a href="https://publications.waset.org/abstracts/23226/non-signaling-chemokine-receptor-ccrl1-and-its-active-counterpart-ccr7-in-prostate-cancer" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/23226.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">469</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4838</span> The Effect of Metformin in Combination with Dexamethasone on the CXCR4 Level in Multiple Myeloma Cell Line</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Seyede%20Sanaz%20Seyedebrahimi">Seyede Sanaz Seyedebrahimi</a>, <a href="https://publications.waset.org/abstracts/search?q=Shima%20Rahimi"> Shima Rahimi</a>, <a href="https://publications.waset.org/abstracts/search?q=Shohreh%20Fakhari"> Shohreh Fakhari</a>, <a href="https://publications.waset.org/abstracts/search?q=Ali%20Jalili"> Ali Jalili</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: CXCR4, as a chemokine receptor, plays well-known roles in various types of cancers. Several studies have been conducted to overcome CXCR4 axis acts in multiple myeloma (MM) pathogenesis and progression. Dexamethasone, a standard treatment for multiple myeloma, has been shown to increase CXCR4 levels in multiple myeloma cell lines. Herein, we focused on the effects of metformin and dexamethasone on CXCR4 at the cellular level and the migration rate of cell lines after exposure to a combination compared to single-agent models. Materials and Method: Multiple myeloma cell lines (U266 and RPMI8226) were cultured with different metformin and dexamethasone concentrations in single-agent and combination models. The simultaneous combination doses were calculated by CompuSyn software. Cell surface and mRNA expression of CXCR4 were determined using flow cytometry and the quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assay, respectively. The Transwell cell migration assay evaluated the migration ability. Results: In concurred with previous studies, our results showed a dexamethasone up-regulation effect on CXCR4 in a dose-dependent manner. Although, the metformin single-agent model could reduce CXCR4 expression of U266 and RPMI8226 in cell surface and mRNA expression level. Moreover, the administration of metformin and dexamethasone simultaneously exerted a higher suppression effect on CXCR4 expression than the metformin single-agent model. The migration rate through the combination model's matrigel membrane was remarkably lower than the metformin and dexamethasone single-agent model. Discussion: According to our findings, the combination of metformin and dexamethasone effectively inhibited dexamethasone-induced CXCR4 expression in multiple myeloma cell lines. As a result, metformin may be counted as an alternative medicine combined with other chemotherapies to combat multiple myeloma. However, more research is required. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=CXCR4" title="CXCR4">CXCR4</a>, <a href="https://publications.waset.org/abstracts/search?q=dexamethasone" title=" dexamethasone"> dexamethasone</a>, <a href="https://publications.waset.org/abstracts/search?q=metformin" title=" metformin"> metformin</a>, <a href="https://publications.waset.org/abstracts/search?q=migration" title=" migration"> migration</a>, <a href="https://publications.waset.org/abstracts/search?q=multiple%20myeloma" title=" multiple myeloma"> multiple myeloma</a> </p> <a href="https://publications.waset.org/abstracts/137004/the-effect-of-metformin-in-combination-with-dexamethasone-on-the-cxcr4-level-in-multiple-myeloma-cell-line" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/137004.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">156</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4837</span> In vitro and vivo Studies for Assessing the Anti-Proliferative, Anti-Migration and Apoptotic Activity of A. squamosa L. Leaves Extract</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Rawan%20Al-Nemari">Rawan Al-Nemari</a>, <a href="https://publications.waset.org/abstracts/search?q=Abdulrahman%20Al-Senaidy"> Abdulrahman Al-Senaidy</a>, <a href="https://publications.waset.org/abstracts/search?q=Abdelhabib%20Semlali"> Abdelhabib Semlali</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background and objectives: The most common cause of death in women worldwide is breast cancer. Regarding all chemotherapy disadvantages and side effects, it’s becoming necessary to identify natural products that target cancer cells with lesser harmful side effects on non-targeted cells and biological environment. Different parts of A. squamosa L., commonly known as custard apple, show varied therapeutic effects. The objective of this study is to investigate in vitro and in vivo, the anti-cancer activity of A. squamosa leaves extract. Methods: The physiological responses using MTT, nucleus staining, and LDH assays were used to evaluate cell survival and proliferation in both ER+ and ER- cells when they were exposed to extract. Monolayer wound repair assay was used to investigate the effect of extracts on cell migration. Apoptotic gene’s expression was investigated by real-time polymerase chain reaction. To study the effect of the extract on the size of tumor, breast cancer induced rats were used. Results: A. squamosa leaves extract showed high anti-proliferative and cytotoxicity effects against different breast cancer cell lines with high concentration, 100 ug/ml. The extracts have reduced the cells wound closure. Polymerase chain reaction revealed downregulation of Bcl-2 and upregulation of Bax. In breast cancer model animal developed in our laboratory, after 4 weeks treatment, treated groups have shown smaller tumor size in comparison with control group (n=4). Conclusion: These results suggest that A. squamosa leaves extract has anti-cancer activity against breast cancer in both in vitro and in vivo, and it may be developed as a potential novel agent to treat breast cancer. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title="apoptosis">apoptosis</a>, <a href="https://publications.waset.org/abstracts/search?q=breast%20cancer" title=" breast cancer"> breast cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=migration" title=" migration"> migration</a>, <a href="https://publications.waset.org/abstracts/search?q=proliferation" title=" proliferation"> proliferation</a> </p> <a href="https://publications.waset.org/abstracts/84443/in-vitro-and-vivo-studies-for-assessing-the-anti-proliferative-anti-migration-and-apoptotic-activity-of-a-squamosa-l-leaves-extract" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/84443.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">147</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4836</span> Characterization of Herberine Hydrochloride Nanoparticles</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Bao-Fang%20Wen">Bao-Fang Wen</a>, <a href="https://publications.waset.org/abstracts/search?q=Meng-Na%20Dai"> Meng-Na Dai</a>, <a href="https://publications.waset.org/abstracts/search?q=Gao-Pei%20Zhu"> Gao-Pei Zhu</a>, <a href="https://publications.waset.org/abstracts/search?q=Chen-Xi%20Zhang"> Chen-Xi Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Jing%20Sun"> Jing Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Xun-Bao%20Yin"> Xun-Bao Yin</a>, <a href="https://publications.waset.org/abstracts/search?q=Yu-Han%20Zhao"> Yu-Han Zhao</a>, <a href="https://publications.waset.org/abstracts/search?q=Hong-Wei%20Sun"> Hong-Wei Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Wei-Fen%20Zhang"> Wei-Fen Zhang</a> </p> <p class="card-text"><strong>Abstract:</strong></p> A drug-loaded nanoparticles containing berberine hydrochloride (BH/FA-CTS-NPs) was prepared. The physicochemical characterizations of BH/FA-CTS-NPs and the inhibitory effect on the HeLa cells were investigated. Folic acid-conjugated chitosan (FA-CTS) was prepared by amino reaction of folic acid active ester and chitosan molecules; BH/FA-CTS-NPs were prepared using ionic cross-linking technique with BH as a model drug. The morphology and particle size were determined by Transmission Electron Microscope (TEM). The average diameters and polydispersity index (PDI) were evaluated by Dynamic Light Scattering (DLS). The interaction between various components and the nanocomplex were characterized by Fourier Transform Infrared Spectroscopy (FT-IR). The entrapment efficiency (EE), drug-loading (DL) and in vitro release were studied by UV spectrophotometer. The effect of cell anti-migratory and anti-invasive actions of BH/FA-CTS-NPs were investigated using MTT assays, wound healing assays, Annexin-V-FITC single staining assays, and flow cytometry, respectively. HeLa nude mice subcutaneously transplanted tumor model was established and treated with different drugs to observe the effect of BH/FA-CTS-NPs in vivo on HeLa bearing tumor. The BH/FA-CTS-NPs prepared in this experiment have a regular shape, uniform particle size, and no aggregation phenomenon. The results of DLS showed that mean particle size, PDI and Zeta potential of BH/FA-CTS NPs were (249.2 ± 3.6) nm, 0.129 ± 0.09, 33.6 ± 2.09, respectively, and the average diameter and PDI were stable in 90 days. The results of FT-IR demonstrated that the characteristic peaks of FA-CTS and BH/FA-CTS-NPs confirmed that FA-CTS cross-linked successfully and BH was encapsulated in NPs. The EE and DL amount were (79.3 ± 3.12) % and (7.24 ± 1.41) %, respectively. The results of in vitro release study indicated that the cumulative release of BH/FA-CTS NPs was (89.48±2.81) % in phosphate-buffered saline (PBS, pH 7.4) within 48h; these results by MTT assays and wund healing assays indicated that BH/FA-CTS NPs not only inhibited the proliferation of HeLa cells in a concentration and time-dependent manner but can induce apoptosis as well. The subcutaneous xenograft tumor formation rate of human cervical cancer cell line HeLa in nude mice was 98% after inoculation for 2 weeks. Compared with BH group and BH/CTS-NPs group, the xenograft tumor growth of BH/FA-CTS-NPs group was obviously slower; the result indicated that BH/FA-CTS-NPs could significantly inhibit the growth of HeLa xenograft tumor. BH/FA-CTS NPs with the sustained release effect could be prepared successfully by the ionic crosslinking method. Considering these properties, block proliferation and impairing the migration of the HeLa cell line, BH/FA-CTS NPs could be an important compound for consideration in the treatment of cervical cancer. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=folic-acid" title="folic-acid">folic-acid</a>, <a href="https://publications.waset.org/abstracts/search?q=chitosan" title=" chitosan"> chitosan</a>, <a href="https://publications.waset.org/abstracts/search?q=berberine%20hydrochloride" title=" berberine hydrochloride"> berberine hydrochloride</a>, <a href="https://publications.waset.org/abstracts/search?q=nanoparticles" title=" nanoparticles"> nanoparticles</a>, <a href="https://publications.waset.org/abstracts/search?q=cervical%20cancer" title=" cervical cancer"> cervical cancer</a> </p> <a href="https://publications.waset.org/abstracts/110474/characterization-of-herberine-hydrochloride-nanoparticles" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/110474.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">122</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4835</span> In vitro and in vivo Antiangiogenic Activity of Girinimbine Isolated from Murraya koenigii</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Venoos%20Iman">Venoos Iman</a>, <a href="https://publications.waset.org/abstracts/search?q=Suzita%20Mohd%20Noor"> Suzita Mohd Noor</a>, <a href="https://publications.waset.org/abstracts/search?q=Syam%20Mohan"> Syam Mohan</a>, <a href="https://publications.waset.org/abstracts/search?q=Mohamad%20Ibrahim%20Noordin"> Mohamad Ibrahim Noordin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Girinimbine, a carbazole alkaloid was isolated from the stem bark and root of Murraya koenigii and its structure and purity was identified by HPLC and LC-MS. Here we report that Girinimbine strongly inhibit angiogenesis activity both in vitro and in vivo. MTT result showed that girinimbine inhibits cell proliferation of the HUVECS cell line in vitro. Result of endothelial cell invasion, migration, tube formation and wound healing assays also demonstrated significant time and does dependent inhibition by girinimbine. Moreover, girinibine mediates its anti-angiogenic activity through up- and down-regulation of angiogenic and anti-aniogenic proteins. Furthermore, anti-angiogenic potential of girinimbine was evidenced in vivo on zebrafish model. Girinimbine inhibited neo-vessels formation in zebrafish embryos during 24 hours exposure time. Together, these results demonstrated for the first time that girinimbine could effectively suppress angiogenesis and strongly suggest that it might be a novel angiogenesis inhibitor. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=anti-angiogenic" title="anti-angiogenic">anti-angiogenic</a>, <a href="https://publications.waset.org/abstracts/search?q=carbazole%20alkaloid" title=" carbazole alkaloid"> carbazole alkaloid</a>, <a href="https://publications.waset.org/abstracts/search?q=girinimbine" title=" girinimbine"> girinimbine</a>, <a href="https://publications.waset.org/abstracts/search?q=zebrafish" title=" zebrafish"> zebrafish</a> </p> <a href="https://publications.waset.org/abstracts/13579/in-vitro-and-in-vivo-antiangiogenic-activity-of-girinimbine-isolated-from-murraya-koenigii" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/13579.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">376</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4834</span> Inhibitory Effect of 13-Butoxyberberine Bromide on Metastasis of Skin Cancer A431 Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Phuriwat%20Laomethakorn">Phuriwat Laomethakorn</a>, <a href="https://publications.waset.org/abstracts/search?q=Siritron%20Samosorn"> Siritron Samosorn</a>, <a href="https://publications.waset.org/abstracts/search?q=Ramida%20Watanapokasin"> Ramida Watanapokasin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Cancer metastasis is the major cause of cancer-related death. Therefore searching for a compound that could inhibit cancer metastasis is necessary. 13-Butoxyberberine bromide is a berberine derivative that has not been reported an anti-metastatic effect on skin cancer cells. This study aimed to investigate the anti-metastatic effect of 13-butoxyberberine bromide on skin cancer A431 cells. The effect of 13-butoxyberberine bromide on A431 cell viability was examined by MTT assay. Suppression of cell migration and invasion in A431 cells were determined by wound healing assay, transwell migration assay, and transwell invasion assay. Metastasis proteins were determined by western blotting. The results demonstrated that 13-butoxyberberine bromide decreased A431 cell viability in a dose-dependent manner. In addition, sub-toxic concentrations of 13-butoxyberberine bromide suppressed cell migration and invasion in A431 cells. In addition, 13-butoxyberberine bromide showed anti-metastatic effects by down-regulated MMP-2 and MMP-9 expression. These findings may be useful in the development of 13-butoxyberberine bromide as an anti-metastatic drug in the future. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=13-butoxyberberine%20bromide" title="13-butoxyberberine bromide">13-butoxyberberine bromide</a>, <a href="https://publications.waset.org/abstracts/search?q=metastasis" title=" metastasis"> metastasis</a>, <a href="https://publications.waset.org/abstracts/search?q=skin%20cancer" title=" skin cancer"> skin cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=MMP" title=" MMP"> MMP</a> </p> <a href="https://publications.waset.org/abstracts/158142/inhibitory-effect-of-13-butoxyberberine-bromide-on-metastasis-of-skin-cancer-a431-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/158142.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">104</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4833</span> Hsa-miR-326 Functions as a Tumor Suppressor in Non-Small Cell Lung Cancer through Targeting CCND1</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Cheng-Cao%20Sun">Cheng-Cao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shu-Jun%20Li"> Shu-Jun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng%20Zhang"> Feng Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=De-Jia%20Li"> De-Jia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Hsa-miRNA-326 (miR-326) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-326 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-326 on the development of NSCLC. The results indicated that miR-326 was significantly down-regulated in primary tumor tissues and very low levels were found in NSCLC cell lines. Ectopic expression of miR-326 in NSCLC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4, and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-326 induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-326 inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene CCND1 was revealed to be a putative target of miR-326, which was inversely correlated with miR-326 expression in NSCLC. Taken together, our results demonstrated that miR-326 played a pivotal role on NSCLC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic CCND1. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hsa-miRNA-326%20%28miR-326%29" title="hsa-miRNA-326 (miR-326)">hsa-miRNA-326 (miR-326)</a>, <a href="https://publications.waset.org/abstracts/search?q=cyclin%20D1" title="cyclin D1">cyclin D1</a>, <a href="https://publications.waset.org/abstracts/search?q=non-small%20cell%20lung%20cancer%20%28NSCLC%29" title=" non-small cell lung cancer (NSCLC)"> non-small cell lung cancer (NSCLC)</a>, <a href="https://publications.waset.org/abstracts/search?q=proliferation" title=" proliferation"> proliferation</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title=" apoptosis"> apoptosis</a> </p> <a href="https://publications.waset.org/abstracts/41380/hsa-mir-326-functions-as-a-tumor-suppressor-in-non-small-cell-lung-cancer-through-targeting-ccnd1" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41380.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">306</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4832</span> Sirt1 Activators Promote Skin Cell Regeneration and Cutaneous Wound Healing</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hussain%20Mustatab%20Wahedi">Hussain Mustatab Wahedi</a>, <a href="https://publications.waset.org/abstracts/search?q=Sun%20You%20Kim"> Sun You Kim</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Skin acts as a barrier against the harmful environmental factors. Integrity and timely recovery of the skin from injuries and harmful effects of radiations is thus very important. This study aimed to investigate the importance of Sirt1 in the recovery of skin from UVB-induced damage and cutaneous wounds by using natural and synthetic novel Sirt1 activators. Juglone, known as a natural Pin1 inhibitor, and NED416 a novel synthetic Sirt1 activator were checked for their ability to regulate the expression and activity of Sirt1 and hence photo-damage and wound healing in cultured skin cells (NHDF and HaCaT cells) and mouse model by using Sirt1 siRNA knockdown, cell migration assay, GST-Pulldown assay, western blot analysis, tube formation assay, and immunohistochemistry. Interestingly, Sirt1 knockdown inhibited skin cell migration in vitro. Juglone up regulated the expression of Sirt1 in both the cell lines under normal and UVB irradiated conditions, enhanced Sirt1 activity and increased the cell viability by reducing reactive oxygen species synthesis and apoptosis. Juglone promoted wound healing by increasing cell migration and angiogenesis through Cdc42/Rac1/PAK, MAPKs and Smad pathways in skin cells. NED416 upregulated Sirt1 expression in HaCaT and NHDF cells as well as increased Sirt1 activity. NED416 promoted the process of wound healing in early as well as later stages by increasing macrophage recruitment, skin cell migration, and angiogenesis through Cdc42/Rac1 and MAPKs pathways. So, both these compounds activated Sirt1 and promoted the process of wound healing thus pointing towards the possible role of Sirt1 in skin regeneration and wound healing. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=skin%20regeneration" title="skin regeneration">skin regeneration</a>, <a href="https://publications.waset.org/abstracts/search?q=wound%20healing" title=" wound healing"> wound healing</a>, <a href="https://publications.waset.org/abstracts/search?q=Sirt1" title=" Sirt1"> Sirt1</a>, <a href="https://publications.waset.org/abstracts/search?q=UVB%20light" title=" UVB light"> UVB light</a> </p> <a href="https://publications.waset.org/abstracts/84195/sirt1-activators-promote-skin-cell-regeneration-and-cutaneous-wound-healing" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/84195.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">188</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4831</span> DNA Fragmentation and Apoptosis in Human Colorectal Cancer Cell Lines by Sesamum indicum Dried Seeds</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mohd%20Farooq%20Naqshbandi">Mohd Farooq Naqshbandi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The four fractions of aqueous extract of Sesame Seeds (Sesamum indicum L.) were studied for invitro DNA fragmentation, cell migration, and cellular apoptosis on SW480 and HTC116 human colorectal cancer cell lines. The seeds of Sesamum indicum were extracted with six solvents, including Methanol, Ethanol, Aqueous, Chloroform, Acetonitrile, and Hexane. The aqueous extract (IC₅₀ value 154 µg/ml) was found to be the most active in terms of cytotoxicity with SW480 human colorectal cancer cell lines. Further fractionation of this aqueous extract on flash chromatography gave four fractions. These four fractions were studied for anticancer and DNA binding studies. Cell viability was assessed by colorimetric assay (MTT). IC₅₀ values for all these four fractions ranged from 137 to 548 µg/mL for the HTC116 cancer cell line and 141 to 402 µg/mL for the SW480 cancer cell line. The four fractions showed good anticancer and DNA binding properties. The DNA binding constants ranged from 10.4 ×10⁴ 5 to 28.7 ×10⁴, showing good interactions with DNA. The DNA binding interactions were due to intercalative and π-π electron forces. The results indicate that aqueous extract fractions of sesame showed inhibition of cell migration of SW480 and HTC116 human colorectal cancer cell lines and induced DNA fragmentation and apoptosis. This was demonstrated by calculating the low wound closure percentage in cells treated with these fractions as compared to the control (80%). Morphological features of nuclei of cells treated with fractions revealed chromatin compression, nuclear shrinkage, and apoptotic body formation, which indicate cell death by apoptosis. The flow cytometer of fraction-treated cells of SW480 and HTC116 human colorectal cancer cell lines revealed death due to apoptosis. The results of the study indicate that aqueous extract of sesame seeds may be used to treat colorectal cancer. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sesamum%20indicum" title="Sesamum indicum">Sesamum indicum</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20migration%20inhibition" title=" cell migration inhibition"> cell migration inhibition</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis%20induction" title=" apoptosis induction"> apoptosis induction</a>, <a href="https://publications.waset.org/abstracts/search?q=anticancer%20activity" title=" anticancer activity"> anticancer activity</a>, <a href="https://publications.waset.org/abstracts/search?q=colorectal%20cancer" title=" colorectal cancer"> colorectal cancer</a> </p> <a href="https://publications.waset.org/abstracts/156154/dna-fragmentation-and-apoptosis-in-human-colorectal-cancer-cell-lines-by-sesamum-indicum-dried-seeds" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/156154.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">88</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4830</span> In vitro Antioxidant Activity of Derris scandens Extract</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Nattawit%20Thiapairat">Nattawit Thiapairat</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Multiple diseases have been linked to excessive levels of free radicals, which cause tissue or cell damage as a result of oxidative stress. Many plants are sources of high antioxidant activity. Derris scandens has a high amount of phenolic and flavonoid contents which demonstrated good biological activities. This study focused on the antioxidant activity of polyphenols extracted from D. scandens. This study performs total flavonoids content and various antioxidant assays, which were 2,2-diphenyl-1-picryl-hydrazyl-hydrate (DPPH) and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging capacity assays. The total flavonoid content of D. scandens extract was determined and expressed as quercetin equivalents (QE)/g measured by the aluminum chloride colorimetric method. The antioxidant activity of D. scandens extract was also determined by DPPH and ABTS assays. In the DPPH assay, vitamin C was used as a positive control, whereas Trolox was used as a positive control in the ABTS assay. The half-maximal inhibitory concentration (IC50) values for D. scandens extract from DPPH and ABTS assays were 41.79 μg/mL ± 0.783 and 29.42 μg/mL ± 0.890, respectively, in the DPPH assay. To conclude, D. scandens extract consists of a high amount of total phenolic content, which exhibits a significant antioxidant activity. However, further investigation regarding antioxidant activity such as SOD, ROS, and RNS scavenging assays and in vivo experiments should be performed. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ABTS%20assay" title="ABTS assay">ABTS assay</a>, <a href="https://publications.waset.org/abstracts/search?q=antioxidant%20activity" title=" antioxidant activity"> antioxidant activity</a>, <a href="https://publications.waset.org/abstracts/search?q=Derris%20scandens" title=" Derris scandens"> Derris scandens</a>, <a href="https://publications.waset.org/abstracts/search?q=DPPH%20assays" title=" DPPH assays"> DPPH assays</a>, <a href="https://publications.waset.org/abstracts/search?q=total%20flavonoid%20content" title=" total flavonoid content"> total flavonoid content</a> </p> <a href="https://publications.waset.org/abstracts/141175/in-vitro-antioxidant-activity-of-derris-scandens-extract" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/141175.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">213</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4829</span> 2D and 3D Breast Cancer Cells Behave Differently to the Applied Free Palbociclib or the Palbociclib-Loaded Nanoparticles </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Maryam%20Parsian">Maryam Parsian</a>, <a href="https://publications.waset.org/abstracts/search?q=Pelin%20Mutlu"> Pelin Mutlu</a>, <a href="https://publications.waset.org/abstracts/search?q=Ufuk%20Gunduz"> Ufuk Gunduz</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Two-dimensional cell culture affords simplicity and low cost, but it has serious limitations; lacking cell-cell and cell-matrix interactions that are present in tissues. Cancer cells grown in 3D culture systems have distinct phenotypes of adhesion, growth, migration, invasion as well as profiles of gene and protein expression. These interactions cause the 3D-cultured cells to acquire morphological and cellular characteristics relevant to in vivo tumors. Palbociclib is a chemotherapeutic agent for the treatment of ER-positive and HER-negative metastatic breast cancer. Poly-amidoamine (PAMAM) dendrimer is a well-defined, special three-dimensional structure and has a multivalent surface and internal cavities that can play an essential role in drug delivery systems. In this study, palbociclib is loaded onto the magnetic PAMAM dendrimer. Hanging droplet method was used in order to form 3D spheroids. The possible toxic effects of both free drug and drug loaded nanoparticles were evaluated in 2D and 3D MCF-7, MD-MB-231 and SKBR-3 breast cancer cell culture models by performing MTT cell viability and Alamar Blue assays. MTT analysis was performed with six different doses from 1000 µg/ml to 25 µg/ml. Drug unloaded PAMAM dendrimer did not demonstrate significant toxicity on all breast cancer cell lines. The results showed that 3D spheroids are clearly less sensitive than 2D cell cultures to free palbociclib. Also, palbociclib loaded PAMAM dendrimers showed more toxic effect than free palbociclib in all cell lines at 2D and 3D cultures. The results suggest that the traditional cell culture method (2D) is insufficient for mimicking the actual tumor tissue. The response of the cancer cells to anticancer drugs is different in the 2D and 3D culture conditions. This study showed that breast cancer cells are more resistant to free palbociclib in 3D cultures than in 2D cultures. However, nanoparticle loaded drugs can be more cytotoxic when compared to free drug. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=2D%20and%203D%20cell%20culture" title="2D and 3D cell culture">2D and 3D cell culture</a>, <a href="https://publications.waset.org/abstracts/search?q=breast%20cancer" title=" breast cancer"> breast cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=palbociclibe" title=" palbociclibe"> palbociclibe</a>, <a href="https://publications.waset.org/abstracts/search?q=PAMAM%20magnetic%20nanoparticles" title=" PAMAM magnetic nanoparticles"> PAMAM magnetic nanoparticles</a> </p> <a href="https://publications.waset.org/abstracts/122615/2d-and-3d-breast-cancer-cells-behave-differently-to-the-applied-free-palbociclib-or-the-palbociclib-loaded-nanoparticles" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/122615.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">149</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4828</span> Hsa-miR-329 Functions as a Tumor Suppressor through Targeting MET in Non-Small Cell Lung Cancer</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Cheng-Cao%20Sun">Cheng-Cao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shu-Jun%20Li"> Shu-Jun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng%20Zhang"> Feng Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=De-Jia%20Li"> De-Jia Li </a> </p> <p class="card-text"><strong>Abstract:</strong></p> MicroRNAs (miRNAs) act as key regulators of multiple cancers. Hsa-miR-329 (miR-329) functions as a tumor suppressor in some malignancies. However, its role on lung cancer remains poorly understood. In this study, we investigated the role of miR-329 on the development of lung cancer. The results indicated that miR-329 was decreased in primary lung cancer tissues compared with matched adjacent normal lung tissues and very low levels were found in a non-small cell lung cancer (NSCLC) cell lines. Ectopic expression of miR-329 in lung cancer cell lines substantially repressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibiting cyclin D1, cyclin D2, and up-regulatiing p57(Kip2) and p21(WAF1/CIP1). In addition, miR-329 promoted NSCLC cell apoptosis, as indicated by up-regulation of key apoptosis gene cleaved caspase-3, and down-regulation of anti-apoptosis gene Bcl2. Moreover, miR-329 inhibited cellular migration and invasiveness through inhibiting matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene MET was revealed to be a putative target of miR-329, which was inversely correlated with miR-329 expression. Furthermore, down-regulation of MET by siRNA performed similar effects to over-expression of miR-329. Collectively, our results demonstrated that miR-329 played a pivotal role in lung cancer through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic MET. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hsa-miRNA-329%28miR-329%29" title="hsa-miRNA-329(miR-329)">hsa-miRNA-329(miR-329)</a>, <a href="https://publications.waset.org/abstracts/search?q=MET" title=" MET"> MET</a>, <a href="https://publications.waset.org/abstracts/search?q=non-small%20cell%20lung%20cancer%20%28NSCLC%29" title="non-small cell lung cancer (NSCLC)">non-small cell lung cancer (NSCLC)</a>, <a href="https://publications.waset.org/abstracts/search?q=proliferation" title=" proliferation"> proliferation</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title=" apoptosis"> apoptosis</a> </p> <a href="https://publications.waset.org/abstracts/41379/hsa-mir-329-functions-as-a-tumor-suppressor-through-targeting-met-in-non-small-cell-lung-cancer" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41379.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">409</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4827</span> Photobiomodulation Activates WNT/β-catenin Signaling for Wound Healing in an in Vitro Diabetic Wound Model</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Dimakatso%20B.%20Gumede">Dimakatso B. Gumede</a>, <a href="https://publications.waset.org/abstracts/search?q=Nicolette%20N.%20Houreld"> Nicolette N. Houreld</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Diabetic foot ulcers (DFUs) are a complication of diabetes mellitus (DM), a metabolic disease caused by insulin resistance or insufficiency, resulting in hyperglycaemia and low-grade chronic inflammation. Current therapies for treating DFUs include wound debridement, glycaemic control, and wound dressing. However, these therapies are moderately effective as there is a recurrence of these ulcers and an increased risk of lower limb amputations. Photobiomodulation (PBM), which is the application of non-invasive low-level light for wound healing at the spectrum of 660-1000 nm, has shown great promise in accelerating the healing of chronic wounds. However, its underlying mechanisms are not clearly defined. Studies have indicated that PBM induces wound healing via the activation of signaling pathways that are involved in tissue repair, such as the transforming growth factor-β (TGF-β). However, other signaling pathways, such as the WNT/β-catenin pathway, which is also critical for wound repair, have not been investigated. This study aimed to elucidate if PBM at 660 nm and a fluence of 5 J/cm² activates the WNT/β-catenin signaling pathway for wound healing in a diabetic cellular model. Human dermal fibroblasts (WS1) were continuously cultured high-glucose (26.5 mM D-glucose) environment to create a diabetic cellular model. A central scratch was created in the diabetic model to ‘wound’ the cells. The diabetic wounded (DW) cells were thereafter irradiated at 660 nm and a fluence of 5 J/cm². Cell migration, gene expression and protein assays were conducted at 24- and 48-h post-PBM. The results showed that PBM at 660 nm and a fluence of 5 J/cm² significantly increased cell migration in diabetic wounded cells at 24-h post-PBM. The expression of CTNNB1, ACTA2, COL1A1 and COL3A1 genes was also increased in DW cells post-PBM. Furthermore, there was increased cytoplasmic accumulation and nuclear localization of β-catenin at 24 h post-PBM. The findings in this study demonstrate that PBM activates the WNT/β-catenin signaling pathway by inducing the accumulation of β-catenin in diabetic wounded cells, leading to increased cell migration and expression of wound repair markers. These results thus indicate that PBM has the potential to improve wound healing in diabetic ulcers via activation of the WNT/β-catenin signaling pathway. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=wound%20healing" title="wound healing">wound healing</a>, <a href="https://publications.waset.org/abstracts/search?q=diabetic%20ulcers" title=" diabetic ulcers"> diabetic ulcers</a>, <a href="https://publications.waset.org/abstracts/search?q=photobiomodulation" title=" photobiomodulation"> photobiomodulation</a>, <a href="https://publications.waset.org/abstracts/search?q=WNT%2F%CE%B2-catenin" title=" WNT/β-catenin"> WNT/β-catenin</a>, <a href="https://publications.waset.org/abstracts/search?q=signalling%20pathway" title=" signalling pathway"> signalling pathway</a> </p> <a href="https://publications.waset.org/abstracts/188444/photobiomodulation-activates-wntv-catenin-signaling-for-wound-healing-in-an-in-vitro-diabetic-wound-model" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/188444.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">40</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4826</span> Review of the World Migration Report 2020, with a Focus on Migration Due to Climate Change</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sincy%20Wilson">Sincy Wilson</a> </p> <p class="card-text"><strong>Abstract:</strong></p> This article focuses on the data scattered throughout the 2020 Report on migration for a variety of reasons. Despite the fact that climate migrants are no longer recognized on an international or national level, their situation remains unchanged, and many countries have already encountered the problem of people entering their country without permission. With the information presented in the paper, researchers are focusing on climate-induced displacement rather than conflict-related migration. The author finishes by stating that there is no time to waste in recognizing climate migrants. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=climate%20refugees" title="climate refugees">climate refugees</a>, <a href="https://publications.waset.org/abstracts/search?q=climatological%20factors" title=" climatological factors"> climatological factors</a>, <a href="https://publications.waset.org/abstracts/search?q=migration" title=" migration"> migration</a>, <a href="https://publications.waset.org/abstracts/search?q=slow-onset%20migration" title=" slow-onset migration"> slow-onset migration</a> </p> <a href="https://publications.waset.org/abstracts/139956/review-of-the-world-migration-report-2020-with-a-focus-on-migration-due-to-climate-change" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/139956.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">213</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4825</span> In Vitro Antioxidant and Free Radical Scavenging Activity of Phyllanthus Emblica L. Extract</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Benyapa%20Suksuwan">Benyapa Suksuwan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Oxidative stress is identified as the root cause of the development and progression of several diseases as the disproportion of free radicals in the body leads to tissue or cell damage. Polyphenols are the most common antioxidant found in plants and are efficient in capturing oxidative free radicals. Aim of the Study: This study focused on the antioxidant activity of polyphenols extracted from Phyllanthus Emblica L. as oxidative stress plays a vital role in developing and progressing many diseases, including cardiovascular diseases and cancer. Materials and Methods: The plant was extracted using a mixture solvent (ethyl alcohol: water in ratio 8:2). The total phenolic content of P. Emblica extract was determined using the Folin-Cioucalteu method and calculated as gallic acid equivalents (GAE) and various antioxidant assays DPPH and ABTS radical scavenging capacity assays. Results and Discussion: The findings exhibited a strong correlation between antioxidant activity and the total phenol contents. In addition, the IC₅₀ of P. Emblica extract via DPPH and ABTS assays were 68.10 μg/mL ± 0.455, and 49.24 μg/mL ± 0.716, respectively. Furthermore, P. Emblica extract showed antioxidant activities in a concentration-dependent manner. Vitamin C was used as a positive control in the DPPH assay, while Trolox was used as a positive control in the ABTS assay. Conclusions: In conclusion, P. Emblica extract consisted of a high amount of total phenolic content, which possesses potent antioxidant activity. However, further antioxidant activity assays using human cell lines such as SOD, ROS, and RNS scavenging assays and in vitro antioxidant experiments should be performed in order. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=antioxidant" title="antioxidant">antioxidant</a>, <a href="https://publications.waset.org/abstracts/search?q=ABTS%20scavenging" title=" ABTS scavenging"> ABTS scavenging</a>, <a href="https://publications.waset.org/abstracts/search?q=DPPH%20scavenging%20assay" title=" DPPH scavenging assay"> DPPH scavenging assay</a>, <a href="https://publications.waset.org/abstracts/search?q=total%20phenol%20contents%20assay" title=" total phenol contents assay"> total phenol contents assay</a>, <a href="https://publications.waset.org/abstracts/search?q=Phyllanthus%20Emblica%20L" title=" Phyllanthus Emblica L"> Phyllanthus Emblica L</a> </p> <a href="https://publications.waset.org/abstracts/140823/in-vitro-antioxidant-and-free-radical-scavenging-activity-of-phyllanthus-emblica-l-extract" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/140823.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">195</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4824</span> Understanding Neuronal and Glial Cell Behaviour in Multi-Layer Nanofibre Systems to Support the Development of an in vitro Model of Spinal Cord Injury and Personalised Prostheses for Repair </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=H.%20Pegram">H. Pegram</a>, <a href="https://publications.waset.org/abstracts/search?q=R.%20Stevens"> R. Stevens</a>, <a href="https://publications.waset.org/abstracts/search?q=L.%20De%20Girolamo"> L. De Girolamo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aligned electrospun nanofibres act as effective neuronal and glial cell scaffolds that can be layered to contain multiple sheets harboring different cell populations. This allows personalised biofunctional prostheses to be manufactured with both acellular and cellularised layers for the treatment of spinal cord injury. Additionally, the manufacturing route may be configured to produce in-vitro 3D cell based model of spinal cord injury to aid drug development and enhance prosthesis performance. The goal of this investigation was to optimise the multi-layer scaffold design parameters for prosthesis manufacture, to enable the development of multi-layer patient specific implant therapies. The work has also focused on the fabricating aligned nanofibre scaffolds that promote in-vitro neuronal and glial cell population growth, cell-to-cell interaction and long-term survival following trauma to mimic an in-vivo spinal cord lesion. The approach has established reproducible lesions and has identified markers of trauma and regeneration marked by effective neuronal migration across the lesion with glial support. The investigation has advanced the development of an in-vitro model of traumatic spinal cord injury and has identified a route to manufacture prostheses which target the repair spinal cord injury. Evidence collated to investigate the multi-layer concept suggests that physical cues provided by nanofibres provide both a natural extra-cellular matrix (ECM) like environment and controls cell proliferation and migration. Specifically, aligned nanofibre layers act as a guidance system for migrating and elongating neurons. On a larger scale, material type in multi-layer systems also has an influence in inter-layer migration as cell types favour different material types. Results have shown that layering nanofibre membranes create a multi-level scaffold system which can enhance or prohibit cell migration between layers. It is hypothesised that modifying nanofibre layer material permits control over neuronal/glial cell migration. Using this concept, layering of neuronal and glial cells has become possible, in the context of tissue engineering and also modelling in-vitro induced lesions. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=electrospinning" title="electrospinning">electrospinning</a>, <a href="https://publications.waset.org/abstracts/search?q=layering" title=" layering"> layering</a>, <a href="https://publications.waset.org/abstracts/search?q=lesion" title=" lesion"> lesion</a>, <a href="https://publications.waset.org/abstracts/search?q=modeling" title=" modeling"> modeling</a>, <a href="https://publications.waset.org/abstracts/search?q=nanofibre" title=" nanofibre"> nanofibre</a> </p> <a href="https://publications.waset.org/abstracts/91909/understanding-neuronal-and-glial-cell-behaviour-in-multi-layer-nanofibre-systems-to-support-the-development-of-an-in-vitro-model-of-spinal-cord-injury-and-personalised-prostheses-for-repair" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/91909.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">138</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4823</span> Platform Integration for High-Throughput Functional Screening Applications</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Karolis%20Leonavi%C4%8Dius">Karolis Leonavičius</a>, <a href="https://publications.waset.org/abstracts/search?q=Dalius%20Ku%C4%8Diauskas"> Dalius Kučiauskas</a>, <a href="https://publications.waset.org/abstracts/search?q=Dangiras%20Luko%C5%A1ius"> Dangiras Lukošius</a>, <a href="https://publications.waset.org/abstracts/search?q=Arnoldas%20Jasi%C5%ABnas"> Arnoldas Jasiūnas</a>, <a href="https://publications.waset.org/abstracts/search?q=Kostas%20Zdanys"> Kostas Zdanys</a>, <a href="https://publications.waset.org/abstracts/search?q=Rokas%20Stanislovas"> Rokas Stanislovas</a>, <a href="https://publications.waset.org/abstracts/search?q=Emilis%20Gegevi%C4%8Dius"> Emilis Gegevičius</a>, <a href="https://publications.waset.org/abstracts/search?q=%C5%BDana%20Kapustina"> Žana Kapustina</a>, <a href="https://publications.waset.org/abstracts/search?q=Juozas%20Nainys"> Juozas Nainys</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Screening throughput is a common bottleneck in many research areas, including functional genomics, drug discovery, and directed evolution. High-throughput screening techniques can be classified into two main categories: (i) affinity-based screening and (ii) functional screening. The first one relies on binding assays that provide information about the affinity of a test molecule for a target binding site. Binding assays are relatively easy to establish; however, they reveal no functional activity. In contrast, functional assays show an effect triggered by the interaction of a ligand at a target binding site. Functional assays might be based on a broad range of readouts, such as cell proliferation, reporter gene expression, downstream signaling, and other effects that are a consequence of ligand binding. Screening of large cell or gene libraries based on direct activity rather than binding affinity is now a preferred strategy in many areas of research as functional assays more closely resemble the context where entities of interest are anticipated to act. Droplet sorting is the basis of high-throughput functional biological screening, yet its applicability is limited due to the technical complexity of integrating high-performance droplet analysis and manipulation systems. As a solution, the Droplet Genomics Styx platform enables custom droplet sorting workflows, which are necessary for the development of early-stage or complex biological therapeutics or industrially important biocatalysts. The poster will focus on the technical design considerations of Styx in the context of its application spectra. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=functional%20screening" title="functional screening">functional screening</a>, <a href="https://publications.waset.org/abstracts/search?q=droplet%20microfluidics" title=" droplet microfluidics"> droplet microfluidics</a>, <a href="https://publications.waset.org/abstracts/search?q=droplet%20sorting" title=" droplet sorting"> droplet sorting</a>, <a href="https://publications.waset.org/abstracts/search?q=dielectrophoresis" title=" dielectrophoresis"> dielectrophoresis</a> </p> <a href="https://publications.waset.org/abstracts/157364/platform-integration-for-high-throughput-functional-screening-applications" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/157364.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">135</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4822</span> The MicroRNA-2110 Suppressed Cell Proliferation and Migration Capacity in Hepatocellular Carcinoma Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Pelin%20Balcik%20Ercin">Pelin Balcik Ercin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: ZEB transcription factor family member ZEB2, has a role in epithelial to mesenchymal transition during development and metastasis. The altered circulating extracellular miRNAs expression is observed in diseases, and extracellular miRNAs have an important role in cancer cell microenvironment. In ChIP-Seq study, the expression of miR-2110 was found to be regulated by ZEB2. In this study, the effects of miR2110 on cell proliferation and migration of hepatocellular carcinoma (HCC) cells were examined. Material and Methods: SNU398 cells transfected with mimic miR2110 (20nM) (HMI0375, Sigma-Aldrich) and negative control miR (HMC0002, Sigma-Aldrich). MicroRNA isolation was accomplished with miRVANA isolation kit according to manufacturer instructions. cDNA synthesis was performed expression, respectively, and calibrated with Ct of controls. The real-time quantitative PCR (RT-qPCR) reaction was performed using the TaqMan Fast Advanced Master Mix (Thermo Sci.). Ct values of miR2110 were normalized to miR-186-5p and miR16-5p for the intracellular gene. Cell proliferation analysis was analyzed with the xCELLigence RTCA System. Wound healing assay was analyzed with the ImageJ program and relative fold change calculated. Results: The mimic-miR-2110 transfected SNU398 cells nearly nine-fold (log2) more miR-2110 expressed compared to negative control transfected cells. The mimic-miR-2110 transfected HCC cell proliferation significantly inhibited compared to the negative control cells. Furthermore, miR-2110-SNU398 cell migration capacity was relatively four-fold decreased compared to negative control-miR-SNU398 cells. Conclusion: Our results suggest the miR-2110 inhibited cell proliferation and also miR-2110 negatively affect cell migration compared to control groups in HCC cells. These data suggest the complexity of microRNA EMT transcription factors regulation. These initial results are pointed out the predictive biomarker capacity of miR-2110 in HCC. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=epithelial%20to%20mesenchymal%20transition" title="epithelial to mesenchymal transition">epithelial to mesenchymal transition</a>, <a href="https://publications.waset.org/abstracts/search?q=EMT" title=" EMT"> EMT</a>, <a href="https://publications.waset.org/abstracts/search?q=hepatocellular%20carcinoma%20cells" title=" hepatocellular carcinoma cells"> hepatocellular carcinoma cells</a>, <a href="https://publications.waset.org/abstracts/search?q=micro-RNA-2110" title=" micro-RNA-2110"> micro-RNA-2110</a>, <a href="https://publications.waset.org/abstracts/search?q=ZEB2" title=" ZEB2"> ZEB2</a> </p> <a href="https://publications.waset.org/abstracts/127977/the-microrna-2110-suppressed-cell-proliferation-and-migration-capacity-in-hepatocellular-carcinoma-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/127977.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">125</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4821</span> Rauvolfine B Isolated from the Bark of Rauvolfia reflexa (Apocynaceae) Induces Apoptosis through Activation of Caspase-9 Coupled with S Phase Cell Cycle Arrest</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mehran%20Fadaeinasab">Mehran Fadaeinasab</a>, <a href="https://publications.waset.org/abstracts/search?q=Hamed%20Karimian"> Hamed Karimian</a>, <a href="https://publications.waset.org/abstracts/search?q=Najihah%20Mohd%20Hashim"> Najihah Mohd Hashim</a>, <a href="https://publications.waset.org/abstracts/search?q=Hapipah%20Mohd%20Ali"> Hapipah Mohd Ali </a> </p> <p class="card-text"><strong>Abstract:</strong></p> In this study, three indole alkaloids namely; rauvolfine B, macusine B, and isoreserpiline have been isolated from the dichloromethane crude extract of Rauvolfia reflexa bark (Apocynaceae). The structural elucidation of the isolated compounds has been performed using spectral methods such as UV, IR, MS, 1D, and 2D NMR. Rauvolfine B showed anti proliferation activity on HCT-116 cancer cell line, its cytotoxicity induction was observed using MTT assay in eight different cell lines. Annexin-V is serving as a marker for apoptotic cells and the Annexin-V-FITC assay was carried out to observe the detection of cell-surface Phosphatidylserine (PS). Apoptosis was confirmed by using caspase-8 and -9 assays. Cell cycle arrest was also investigated using flowcytometric analysis. rauvolfine B had exhibited significantly higher cytotoxicity against HCT-116 cell line. The treatment significantly arrested HCT-116 cells in the S phase. Together, the results presented in this study demonstrated that rauvolfine B inhibited the proliferation of HCT-116 cells and programmed cell death followed by cell cycle arrest. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=apocynacea" title="apocynacea">apocynacea</a>, <a href="https://publications.waset.org/abstracts/search?q=indole%20alkaloid" title=" indole alkaloid"> indole alkaloid</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title=" apoptosis"> apoptosis</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20cycle%20arrest" title=" cell cycle arrest"> cell cycle arrest</a> </p> <a href="https://publications.waset.org/abstracts/13403/rauvolfine-b-isolated-from-the-bark-of-rauvolfia-reflexa-apocynaceae-induces-apoptosis-through-activation-of-caspase-9-coupled-with-s-phase-cell-cycle-arrest" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/13403.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">334</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4820</span> Anti-TNF: Possibilities of Rising Anti-Phosphorylcholine Antibodies</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Md.%20Mizanur%20Rahman">Md. Mizanur Rahman</a>, <a href="https://publications.waset.org/abstracts/search?q=Anquan%20Liu"> Anquan Liu</a>, <a href="https://publications.waset.org/abstracts/search?q=Anna%20Frosteg%C3%A5rd"> Anna Frostegård</a>, <a href="https://publications.waset.org/abstracts/search?q=Johan%20Frosteg%C3%A5rd"> Johan Frostegård</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The role of the human immune system is essential in cardiovascular diseases and atherosclerosis. Activated cells in atherosclerosis produce abundant amounts of cytokines, but the exact mechanisms involved in the effects of these inflammatory cytokines are not clear in atherosclerosis. In a large clinical cohort, we have previously determined that antibodies against phosphorylcholine (anti-PC) are negatively and independently associated with both development of atherosclerosis and also a low risk of cardiovascular disease. Further, we reported that rheumatoid arthritis patients who were non-responders to TNF-inhibitors, where those with low anti-PC levels. Upon anti-TNF treatment, anti-PC levels increased. We, therefore, hypothesised that proinflammatory cytokines such as TNF could play a role in anti-PC regulation. Peripheral blood mononuclear cells (PBMC) were cultured with or without TNF and anti-TNF. The cell supernatants were collected after six days for ELISA measurements. In separate experiments, cells were cultured for 24 hours in both polystyrene plates and ELISPOT plates under a similar condition for ELISA and ELISPOT assays respectively. Total RNA was extracted after 6 hours of cell culture to perform RT-qPCR. Cell viability was confirmed by trypan blue staining and MTT assays. ELISA measurements detected less than 40% of anti-PC in TNF-treated cells, in comparison to control cells, whereas anti-PC production was recovered by anti-TNF treatment. ELISPOT assays showed that TNF suppresses anti-PC production by inhibiting anti-PC producing B-cells. In addition, RT-qPCR and ELISA showed that TNF also has effects also on B-cell activation as BAFF expression was inhibited by TNF treatment. Atherosclerosis is a major cause of cardiovascular diseases, but anti-PC is a protection marker for atherosclerosis development. Our findings show that TNF is a negative regulator of anti-PC production. Immune modulation and rising of anti-PC could be of major significance for the patients. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=anti-PC" title="anti-PC">anti-PC</a>, <a href="https://publications.waset.org/abstracts/search?q=Anti-TNF" title=" Anti-TNF"> Anti-TNF</a>, <a href="https://publications.waset.org/abstracts/search?q=atherosclerosis" title=" atherosclerosis"> atherosclerosis</a>, <a href="https://publications.waset.org/abstracts/search?q=cardiovascular%20diseases" title=" cardiovascular diseases"> cardiovascular diseases</a>, <a href="https://publications.waset.org/abstracts/search?q=phosphorylecholine" title=" phosphorylecholine"> phosphorylecholine</a> </p> <a href="https://publications.waset.org/abstracts/44750/anti-tnf-possibilities-of-rising-anti-phosphorylcholine-antibodies" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/44750.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">243</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4819</span> The Strategy of the International Organization for Migration in Dealing with the Phenomenon of Migration</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Djehich%20Mohamed%20Yousri">Djehich Mohamed Yousri</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Nowadays, migration has become a phenomenon that attracts the attention of researchers, countries, agencies, and national and international bodies. Wars and climate change, demographics, poverty, natural disasters, and epidemics are all threats that are contributing daily to forcing more people to migrate. There are those who resort to emigration because of the deteriorating political conditions in their country, others resort to emigration to improve their financial situation, and others emigrate from their country for fear of some penalties and judgments issued against them. In the field of migration, becoming a member of the United Nations as a "relevant organization" gives the United Nations a clear mandate on migration. Its primary goal is to facilitate the management of international migration in an orderly and humane manner. In order to achieve this goal, the organization adopts an international policy to meet the challenges posed in the field of migration. This paper attempts to study the structure of this international organization and its strategy in dealing with the phenomenon of international migration. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=international%20organization%20for%20migration" title="international organization for migration">international organization for migration</a>, <a href="https://publications.waset.org/abstracts/search?q=immigrants" title=" immigrants"> immigrants</a>, <a href="https://publications.waset.org/abstracts/search?q=immigrant%20rights" title=" immigrant rights"> immigrant rights</a>, <a href="https://publications.waset.org/abstracts/search?q=resettlement" title=" resettlement"> resettlement</a>, <a href="https://publications.waset.org/abstracts/search?q=migration%20organization%20strategy" title=" migration organization strategy"> migration organization strategy</a> </p> <a 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