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10.1016/j.canlet.2016.01.009 http://scihub22266oqcxt.onion/10.1016/j.canlet.2016.01.009 C4769873!4769873!26801746     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Lett 2016 ; 373 (1): 36-44 Nephropedia Template TP {{tp|p=26801746|t=2016. Overcoming cisplatin resistance of ovarian cancer cells by targeting HIF-1-regulated cancer metabolism |pdf=|usr=}}{{26801746}} gab.com Text Overcoming cisplatin resistance of ovarian cancer cells by targeting HIF-1-regulated cancer metabolism JO: Cancer Lett http://www.kidney.de/pget.php?&tw=1&pmid=26801746 #FOAvip Cisplatin is currently one of the most effective chemotherapeutic drugs used for treating ovarian cancer; however, resistance to cisplatin is common. In this study, we explored an experimental strategy for overcoming cisplatin resistance of human ovarian cancer from the new perspective of cancer cell metabolism. By using two pairs of genetically matched cisplatin-sensitive and cisplatin-resistant ovarian cancer cell lines, we tested the hypothesis that downregulating hypoxia-inducible factor-1 (HIF-1), which regulates metabolic enzymes involved in glycolysis, is a promising strategy for overcoming cisplatin resistance of human ovarian cancer cells. We found that cisplatin downregulated the level of the regulatable ? subunit of HIF-1, HIF-1?, in cisplatin-sensitive ovarian cancer cells through enhancing HIF-1? degradation but did not downregulate HIF-1? in their cisplatin-resistant counterparts. Overexpression of a degradation-resistant HIF-1? (HIF-1? ?ODD) reduced cisplatin-induced apoptosis in cisplatin-sensitive cells, whereas genetic knockdown of HIF-1? or pharmacological promotion of HIF-1? degradation enhanced response to cisplatin in both cisplatin-sensitive and cisplatin-resistant ovarian cancer cells. We further demonstrated that knockdown of HIF-1? improved the response of cisplatin-resistant ovarian cancer cells to cisplatin by redirecting the aerobic glycolysis in the resistant cancer cells towards mitochondrial oxidative phosphorylation, leading to cell death through overproduction of reactive oxygen species. Our findings suggest that the HIF-1?-regulated cancer metabolism pathway could be a novel target for overcoming cisplatin resistance in ovarian cancer. Twit Text FOAVip Overcoming cisplatin resistance of ovarian cancer cells by targeting HIF-1-regulated cancer metabolism ????Cancer Lett http://www.kidney.de/pget.php?&tw=1&pmid=26801746 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26801746 #FOAvip English Wikipedia <ref>{{Cite pmid|26801746}}</ref> Overcoming cisplatin resistance of ovarian cancer cells by targeting HIF-1-regulated cancer metabolism #MMPMID26801746 Ai Z; Lu Y; Qiu S; Fan Z Cancer Lett 2016[Apr]; 373 (1): 36-44 PMID26801746show ga Cisplatin is currently one of the most effective chemotherapeutic drugs used for treating ovarian cancer; however, resistance to cisplatin is common. In this study, we explored an experimental strategy for overcoming cisplatin resistance of human ovarian cancer from the new perspective of cancer cell metabolism. By using two pairs of genetically matched cisplatin-sensitive and cisplatin-resistant ovarian cancer cell lines, we tested the hypothesis that downregulating hypoxia-inducible factor-1 (HIF-1), which regulates metabolic enzymes involved in glycolysis, is a promising strategy for overcoming cisplatin resistance of human ovarian cancer cells. We found that cisplatin downregulated the level of the regulatable ? subunit of HIF-1, HIF-1?, in cisplatin-sensitive ovarian cancer cells through enhancing HIF-1? degradation but did not downregulate HIF-1? in their cisplatin-resistant counterparts. Overexpression of a degradation-resistant HIF-1? (HIF-1? ?ODD) reduced cisplatin-induced apoptosis in cisplatin-sensitive cells, whereas genetic knockdown of HIF-1? or pharmacological promotion of HIF-1? degradation enhanced response to cisplatin in both cisplatin-sensitive and cisplatin-resistant ovarian cancer cells. We further demonstrated that knockdown of HIF-1? improved the response of cisplatin-resistant ovarian cancer cells to cisplatin by redirecting the aerobic glycolysis in the resistant cancer cells towards mitochondrial oxidative phosphorylation, leading to cell death through overproduction of reactive oxygen species. Our findings suggest that the HIF-1?-regulated cancer metabolism pathway could be a novel target for overcoming cisplatin resistance in ovarian cancer. äOvercoming cisplatin resistance of ovarian cancer cells by targeting H(epmc).pdf DeepDyve Pubget Overpricing