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10.1038/srep12410 http://scihub22266oqcxt.onion/10.1038/srep12410 C4502431!4502431 !26174737     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26174737 &cmd=llinks): Failed to open stream: HTTP request failed! 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Copper depletion inhibits CoCl2-induced aggressive phenotype of MCF-7 cells via downregulation of HIF-1 and inhibition of Snail/Twist-mediated epithelial-mesenchymal transition |pdf=|usr=}}{{26174737 }} gab.com Text Copper depletion inhibits CoCl2-induced aggressive phenotype of MCF-7 cells via downregulation of HIF-1 and inhibition of Snail/Twist-mediated epithelial-mesenchymal transition JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26174737 #FOAvip Copper, a strictly regulated trace element, is essential for many physiological processes including angiogenesis. Dysregulated angiogenesis has been associated with increased copper in tumors, and thus copper chelators have been used to inhibit tumor angiogenesis. However, it remains unclear whether copper has any effect on epithelial-mesenchymal transition (EMT). Using CoCl2-induced EMT of human breast carcinoma MCF-7 cells, we found that TEPA, a copper chelator, inhibited EMT-like cell morphology and cytoskeleton arrangement triggered by CoCl2; decreased the expression of vimentin and fibronectin, markers typical of EMT; inhibited HIF-1 activation and HIF1-? accumulation in nuclear; and down-regulated the expression of hypoxia-associated transcription factors, Snail and Twist1. Moreover, knockdown copper transport protein, Ctr1, also inhibited CoCl2-induced EMT and reversed the mesenchymal phenotype. In EMT6 xenograft mouse models, TEPA administration inhibited the tumor growth and increased mice survival. Immunohistochemical analysis of the xenograft further demonstrated that TEPA administration significantly inhibited tumor angiogenesis, down-regulated hypoxia-induced transcription factors, Snail and Twist1, leading to decreased transactivation of EMT-associated marker genes, vimentin and fibronectin. These results indicate that TEPA inhibits CoCl2-induced EMT most likely via HIF1-?-Snail/Twist signaling pathway, and copper depletion may be exploited as a therapeutic for breast cancer. Twit Text FOAVip Copper depletion inhibits CoCl2-induced aggressive phenotype of MCF-7 cells via downregulation of HIF-1 and inhibition of Snail/Twist-mediated epithelial-mesenchymal transition ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26174737 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26174737 #FOAvip English Wikipedia <ref>{{Cite pmid|26174737 }}</ref> Copper depletion inhibits CoCl2-induced aggressive phenotype of MCF-7 cells via downregulation of HIF-1 and inhibition of Snail/Twist-mediated epithelial-mesenchymal transition #MMPMID26174737 Li S ; Zhang J ; Yang H ; Wu C ; Dang X ; Liu Y Sci Rep 2015[Jul]; 5 (ä): 12410 PMID26174737 show ga Copper, a strictly regulated trace element, is essential for many physiological processes including angiogenesis. Dysregulated angiogenesis has been associated with increased copper in tumors, and thus copper chelators have been used to inhibit tumor angiogenesis. However, it remains unclear whether copper has any effect on epithelial-mesenchymal transition (EMT). Using CoCl2-induced EMT of human breast carcinoma MCF-7 cells, we found that TEPA, a copper chelator, inhibited EMT-like cell morphology and cytoskeleton arrangement triggered by CoCl2; decreased the expression of vimentin and fibronectin, markers typical of EMT; inhibited HIF-1 activation and HIF1-? accumulation in nuclear; and down-regulated the expression of hypoxia-associated transcription factors, Snail and Twist1. Moreover, knockdown copper transport protein, Ctr1, also inhibited CoCl2-induced EMT and reversed the mesenchymal phenotype. In EMT6 xenograft mouse models, TEPA administration inhibited the tumor growth and increased mice survival. Immunohistochemical analysis of the xenograft further demonstrated that TEPA administration significantly inhibited tumor angiogenesis, down-regulated hypoxia-induced transcription factors, Snail and Twist1, leading to decreased transactivation of EMT-associated marker genes, vimentin and fibronectin. These results indicate that TEPA inhibits CoCl2-induced EMT most likely via HIF1-?-Snail/Twist signaling pathway, and copper depletion may be exploited as a therapeutic for breast cancer. |Animals [MESH] |Antineoplastic Agents, Alkylating/therapeutic use/toxicity [MESH] |Breast Neoplasms/drug therapy/pathology [MESH] |Cation Transport Proteins/antagonists & inhibitors/genetics/metabolism [MESH] |Cell Adhesion [MESH] |Cell Line, Tumor [MESH] |Cell Movement/drug effects [MESH] |Cell Polarity [MESH] |Cobalt/chemistry/pharmacology [MESH] |Copper Transporter 1 [MESH] |Copper/*metabolism [MESH] |Down-Regulation/drug effects [MESH] |Epithelial-Mesenchymal Transition/drug effects [MESH] |Female [MESH] |Fibronectins/genetics/metabolism [MESH] |Humans [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism [MESH] |Immunohistochemistry [MESH] |MCF-7 Cells [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Nuclear Proteins/antagonists & inhibitors/*metabolism [MESH] |Phenotype [MESH] |RNA Interference [MESH] |RNA, Small Interfering/metabolism [MESH] |Signal Transduction/drug effects [MESH] |Snail Family Transcription Factors [MESH] |Transcription Factors/antagonists & inhibitors/*metabolism [MESH] |Transcriptional Activation [MESH] |Transplantation, Heterologous [MESH] |Triethylenephosphoramide/therapeutic use/toxicity [MESH] |Twist-Related Protein 1/antagonists & inhibitors/*metabolism [MESH]Copper depletion inhibits CoCl2-induced aggressive phenotype of MCF-7 (epmc).pdf DeepDyve Pubget Overpricing