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10.3390/cancers8040040 http://scihub22266oqcxt.onion/10.3390/cancers8040040 C4846849!4846849!27023612     free     free     free       Cancers+(Basel) 2016 ; 8 (4): ä Nephropedia Template TP {{tp|p=27023612|t=2016. Mitochondrial Redox Signaling and Tumor Progression |pdf=|usr=}}{{27023612}} gab.com Text Mitochondrial Redox Signaling and Tumor Progression JO: Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=27023612 #FOAvip Cancer cell can reprogram their energy production by switching mitochondrial oxidative phosphorylation to glycolysis. However, mitochondria play multiple roles in cancer cells, including redox regulation, reactive oxygen species (ROS) generation, and apoptotic signaling. Moreover, these mitochondrial roles are integrated via multiple interconnected metabolic and redox sensitive pathways. Interestingly, mitochondrial redox proteins biphasically regulate tumor progression depending on cellular ROS levels. Low level of ROS functions as signaling messengers promoting cancer cell proliferation and cancer invasion. However, anti-cancer drug-initiated stress signaling could induce excessive ROS, which is detrimental to cancer cells. Mitochondrial redox proteins could scavenger basal ROS and function as ?tumor suppressors? or prevent excessive ROS to act as ?tumor promoter?. Paradoxically, excessive ROS often also induce DNA mutations and/or promotes tumor metastasis at various stages of cancer progression. Targeting redox-sensitive pathways and transcriptional factors in the appropriate context offers great promise for cancer prevention and therapy. However, the therapeutics should be cancer-type and stage-dependent. Twit Text FOAVip Mitochondrial Redox Signaling and Tumor Progression ????Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=27023612 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27023612 #FOAvip English Wikipedia <ref>{{Cite pmid|27023612}}</ref> Mitochondrial Redox Signaling and Tumor Progression #MMPMID27023612 Chen Y; Zhang H; Zhou HJ; Ji W; Min W Cancers (Basel) 2016[Apr]; 8 (4): ä PMID27023612show ga Cancer cell can reprogram their energy production by switching mitochondrial oxidative phosphorylation to glycolysis. However, mitochondria play multiple roles in cancer cells, including redox regulation, reactive oxygen species (ROS) generation, and apoptotic signaling. Moreover, these mitochondrial roles are integrated via multiple interconnected metabolic and redox sensitive pathways. Interestingly, mitochondrial redox proteins biphasically regulate tumor progression depending on cellular ROS levels. Low level of ROS functions as signaling messengers promoting cancer cell proliferation and cancer invasion. However, anti-cancer drug-initiated stress signaling could induce excessive ROS, which is detrimental to cancer cells. Mitochondrial redox proteins could scavenger basal ROS and function as ?tumor suppressors? or prevent excessive ROS to act as ?tumor promoter?. Paradoxically, excessive ROS often also induce DNA mutations and/or promotes tumor metastasis at various stages of cancer progression. Targeting redox-sensitive pathways and transcriptional factors in the appropriate context offers great promise for cancer prevention and therapy. However, the therapeutics should be cancer-type and stage-dependent. äMitochondrial Redox Signaling and Tumor Progression (epmc).pdf DeepDyve Pubget Overpricing