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10.1186/1471-2407-13-108 http://scihub22266oqcxt.onion/10.1186/1471-2407-13-108 23496980!3614870!23496980     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23496980&cmd=llinks): Failed to open stream: HTTP request failed! 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Hypoxia induces epithelial-mesenchymal transition via activation of SNAI1 by hypoxia-inducible factor -1alpha in hepatocellular carcinoma |pdf=|usr=}}{{23496980}} gab.com Text Hypoxia induces epithelial-mesenchymal transition via activation of SNAI1 by hypoxia-inducible factor -1alpha in hepatocellular carcinoma JO: BMC Cancer http://www.kidney.de/pget.php?&tw=1&pmid=23496980 #FOAvip BACKGROUND: High invasion and metastasis are the primary factors causing poor prognosis of patients with hepatocellular carcinoma (HCC). However, the molecular mechanisms underlying these biological behaviors have not been completely elucidated. In this study, we investigate the molecular mechanism by which hypoxia promotes HCC invasion and metastasis through inducing epithelial-mesenchymal transition (EMT). METHODS: The expression of EMT markers was analyzed by immunohistochemistry. Effect of hypoxia on induction of EMT and ability of cell migration and invasion were performed. Luciferase reporter system was used for evaluation of Snail regulation by hypoxia-inducible factor -1alpha (HIF-1alpha). RESULTS: We found that overexpression of HIF-1alpha was observed in HCC liver tissues and was related to poor prognosis of HCC patients. HIF-1alpha expression profile was correlated with the expression levels of SNAI1, E-cadherin, N-cadherin and Vimentin. Hypoxia was able to induce EMT and enhance ability of invasion and migration in HCC cells. The same phenomena were also observed in CoCl2-treated cells. The shRNA-mediated HIF-1alpha suppression abrogated CoCl2-induced EMT and reduced ability of migration and invasion in HCC cells. Luciferase assay showed that HIF-1alpha transcriptional regulated the expression of SNAI1 based on two hypoxia response elements (HREs) in SNAI1 promoter. CONCLUSIONS: We demonstrated that hypoxia-stabilized HIF1alpha promoted EMT through increasing SNAI1 transcription in HCC cells. This data provided a potential therapeutic target for HCC treatment. Twit Text FOAVip Hypoxia induces epithelial-mesenchymal transition via activation of SNAI1 by hypoxia-inducible factor -1alpha in hepatocellular carcinoma ????BMC Cancer http://www.kidney.de/pget.php?&tw=1&pmid=23496980 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23496980 #FOAvip English Wikipedia <ref>{{Cite pmid|23496980}}</ref> Hypoxia induces epithelial-mesenchymal transition via activation of SNAI1 by hypoxia-inducible factor -1alpha in hepatocellular carcinoma #MMPMID23496980 Zhang L; Huang G; Li X; Zhang Y; Jiang Y; Shen J; Liu J; Wang Q; Zhu J; Feng X; Dong J; Qian C BMC Cancer 2013[Mar]; 13 (ä): 108 PMID23496980show ga BACKGROUND: High invasion and metastasis are the primary factors causing poor prognosis of patients with hepatocellular carcinoma (HCC). However, the molecular mechanisms underlying these biological behaviors have not been completely elucidated. In this study, we investigate the molecular mechanism by which hypoxia promotes HCC invasion and metastasis through inducing epithelial-mesenchymal transition (EMT). METHODS: The expression of EMT markers was analyzed by immunohistochemistry. Effect of hypoxia on induction of EMT and ability of cell migration and invasion were performed. Luciferase reporter system was used for evaluation of Snail regulation by hypoxia-inducible factor -1alpha (HIF-1alpha). RESULTS: We found that overexpression of HIF-1alpha was observed in HCC liver tissues and was related to poor prognosis of HCC patients. HIF-1alpha expression profile was correlated with the expression levels of SNAI1, E-cadherin, N-cadherin and Vimentin. Hypoxia was able to induce EMT and enhance ability of invasion and migration in HCC cells. The same phenomena were also observed in CoCl2-treated cells. The shRNA-mediated HIF-1alpha suppression abrogated CoCl2-induced EMT and reduced ability of migration and invasion in HCC cells. Luciferase assay showed that HIF-1alpha transcriptional regulated the expression of SNAI1 based on two hypoxia response elements (HREs) in SNAI1 promoter. CONCLUSIONS: We demonstrated that hypoxia-stabilized HIF1alpha promoted EMT through increasing SNAI1 transcription in HCC cells. This data provided a potential therapeutic target for HCC treatment. |Cadherins/metabolism[MESH] |Carcinoma, Hepatocellular/*genetics/metabolism/mortality[MESH] |Cell Cycle[MESH] |Cell Line, Tumor[MESH] |Cell Movement/drug effects/genetics[MESH] |Cobalt/pharmacology[MESH] |Epithelial-Mesenchymal Transition/*genetics[MESH] |Gene Expression[MESH] |Gene Expression Regulation, Neoplastic[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*genetics/metabolism[MESH] |Hypoxia/*genetics[MESH] |Liver Neoplasms/*genetics/metabolism/mortality[MESH] |Prognosis[MESH] |Protein Stability/drug effects[MESH] |Snail Family Transcription Factors[MESH] |Transcription Factors/*genetics/metabolism[MESH] |Transcription, Genetic[MESH]Hypoxia induces epithelial-mesenchymal transition via activation of SN(epmc).pdf DeepDyve Pubget Overpricing