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Keywords {🔍}

cancer, pubmed, article, cells, stem, google, scholar, cell, cas, resveratrol, central, human, sulindac, rahbarghazi, tabriz, medical, sciences, research, transition, university, reza, endothelial, nourazarian, avci, colorectal, content, colon, alireza, çığır, biray, res, author, privacy, cookies, data, treatment, rezabakhsh, autophagy, resistance, signaling, access, iran, information, publish, search, pouyafar, emel, sokullu, potential, factor,

Topics {✒️}

çığır biray avci targeting epithelial–mesenchymal transition month download article/chapter mesenchymal–epithelial transition epithelial–mesenchymal transition mesenchymal-endothelial transition cancer stem cells mir-21/akt/β-catenin ht-29 cancer cells resveratrol-induced cell death abc transporter bcrp1/abcg2 furan-2-carboxamide induces g2/ human ovarian cancer cancer stem cell cancer stem cell harvard-mit health sciences real-time pcr assay endothelial differentiation colon-derived cells alireza nourazarian original draft/data collection stem cells real-time pcr analysis autophagy signaling genes full article pdf endothelial induction medium epithelial transition check access instant access vascular endothelial cadherin colon cancer prevention milad zadi heydarabad longitudinal transcriptional response imam reza st reza rahbarghazi related subjects resveratrol suppresses growth cancer stem tissue research aims sulindac inhibits activation privacy choices/manage cookies induces autophagy clin colorectal cancer colorectal cancer rates autophagy signaling glycosylation-related genes angiogenic factor ykl-40 article pouyafar wnt signaling pathway von willebrand factor

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         headline:Treatment of cancer stem cells from human colon adenocarcinoma cell line HT-29 with resveratrol and sulindac induced mesenchymal-endothelial transition rate
         description:In the current experiment, the combined regime of resveratrol and a Wnt-3a inhibitor, sulindac, were examined on the angiogenic potential of cancer stem cells from human colon adenocarcinoma cell line HT-29 during 7 days. Cancer stem cells were enriched via a magnetic-activated cell sorter technique and cultured in endothelial induction medium containing sulindac and resveratrol. Expression of endothelial markers such as the von Willebrand factor (vWF) and vascular endothelial cadherin (VE-cadherin) and genes participating in mesenchymal-to-epithelial transition was studied by real-time PCR assay. Protein levels of Wnt-3a and angiogenic factor YKL-40 were examined by western blotting. ELISA was used to determine the level of N-acetylgalactosaminyltransferase 11 (GALNT11) during mesenchymal-endothelial transition. Autophagy status was monitored by PCR array under treatment with the resveratrol plus sulindac. Results showed that resveratrol and sulindac had the potential to decrease the cell survival of HT-29 cancer cells and the clonogenic capacity of cancer stem cells compared with the control (p < 0.05). The expression of VE-cadherin and vWF was induced in cancer stem cells incubated with endothelial differentiation medium enriched with resveratrol (p < 0.05). Interestingly, the Wnt-3a level was increased in the presence of resveratrol and sulindac (p < 0.05). YKL-40 was reduced after cell exposure to sulindac and resveratrol. The intracellular content of resistance factor GALNT11 was diminished after treatment with resveratrol (p < 0.05). Resveratrol had the potential to induce the transcription of autophagy signaling genes in cancer stem cells during endothelial differentiation (p < 0.05). These data show that resveratrol could increase cancer stem cell trans-differentiation toward endothelial lineage while decrease cell resistance by modulation of autophagy signaling and GALNT11 synthesis.
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      headline:Treatment of cancer stem cells from human colon adenocarcinoma cell line HT-29 with resveratrol and sulindac induced mesenchymal-endothelial transition rate
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         Sulindac
         Resveratrol
         Endothelial differentiation
         Autophagy
         Human Genetics
         Proteomics
         Molecular Medicine
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