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10.7150/thno.20861 http://scihub22266oqcxt.onion/10.7150/thno.20861 C5596433!5596433!28912885     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28912885&cmd=llinks): Failed to open stream: HTTP request failed! 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Brusatol-Mediated Inhibition of c-Myc Increases HIF-1? Degradation and Causes Cell Death in Colorectal Cancer under Hypoxia |pdf=|usr=}}{{28912885}} gab.com Text Brusatol-Mediated Inhibition of c-Myc Increases HIF-1 Degradation and Causes Cell Death in Colorectal Cancer under Hypoxia JO: Theranostics http://www.kidney.de/pget.php?&tw=1&pmid=28912885 #FOAvip HIF-1 (hypoxia-inducible factor-1) regulates the expression of ~100 genes involved in angiogenesis, metastasis, tumor growth, chemoresistance and radioresistance, underscoring the growing interest in targeting HIF-1 for cancer control. In the present study, we investigated the molecular mechanisms underlying brusatol-induced HIF-1? degradation and cell death in colorectal cancer under hypoxia (0.5% O2). Under hypoxia, pretreatment of cancer cells with brusatol increased HIF-1? degradation and cancer cell death in a dose-dependent manner. This effect was mediated by activation of prolyl hydroxylases (PHDs), as evidenced by the block of brusatol-induced HIF-1? degradation and cancer cell death by both pharmacological inhibition and siRNA-mediated knockdown of PHDs. In addition, a ferrous iron chelator (2,2'-bypyridyl) blocked brusatol-induced degradation of HIF-1? and cancer cell death in hypoxia by inhibiting PHD activation. We further found that brusatol inhibited c-Myc expression, and showed that overexpression of c-Myc prevented brusatol-induced degradation of HIF-1? and cancer cell death by increasing mitochondrial ROS production and subsequent ROS-mediated transition of ferrous iron to ferric iron. Consistent with these results, treatment of tumor-bearing mice with brusatol significantly suppressed tumor growth by promoting PHD-mediated HIF-1? degradation. Collectively, our results suggest that brusatol-mediated inhibition of c-Myc/ROS signaling pathway increases HIF-1? degradation by promoting PHD activity and induces cell death in colorectal cancer under hypoxia Twit Text FOAVip Brusatol-Mediated Inhibition of c-Myc Increases HIF-1 Degradation and Causes Cell Death in Colorectal Cancer under Hypoxia ????Theranostics http://www.kidney.de/pget.php?&tw=1&pmid=28912885 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28912885 #FOAvip English Wikipedia <ref>{{Cite pmid|28912885}}</ref> Brusatol-Mediated Inhibition of c-Myc Increases HIF-1? Degradation and Causes Cell Death in Colorectal Cancer under Hypoxia #MMPMID28912885 Oh ET; Kim CW; Kim HG; Lee JS; Park HJ Theranostics 2017[]; 7 (14): 3415-31 PMID28912885show ga HIF-1 (hypoxia-inducible factor-1) regulates the expression of ~100 genes involved in angiogenesis, metastasis, tumor growth, chemoresistance and radioresistance, underscoring the growing interest in targeting HIF-1 for cancer control. In the present study, we investigated the molecular mechanisms underlying brusatol-induced HIF-1? degradation and cell death in colorectal cancer under hypoxia (0.5% O2). Under hypoxia, pretreatment of cancer cells with brusatol increased HIF-1? degradation and cancer cell death in a dose-dependent manner. This effect was mediated by activation of prolyl hydroxylases (PHDs), as evidenced by the block of brusatol-induced HIF-1? degradation and cancer cell death by both pharmacological inhibition and siRNA-mediated knockdown of PHDs. In addition, a ferrous iron chelator (2,2'-bypyridyl) blocked brusatol-induced degradation of HIF-1? and cancer cell death in hypoxia by inhibiting PHD activation. We further found that brusatol inhibited c-Myc expression, and showed that overexpression of c-Myc prevented brusatol-induced degradation of HIF-1? and cancer cell death by increasing mitochondrial ROS production and subsequent ROS-mediated transition of ferrous iron to ferric iron. Consistent with these results, treatment of tumor-bearing mice with brusatol significantly suppressed tumor growth by promoting PHD-mediated HIF-1? degradation. Collectively, our results suggest that brusatol-mediated inhibition of c-Myc/ROS signaling pathway increases HIF-1? degradation by promoting PHD activity and induces cell death in colorectal cancer under hypoxia äBrusatol-Mediated Inhibition of c-Myc Increases HIF-1? Degradation and(epmc).pdf DeepDyve Pubget Overpricing