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10.1152/ajpcell.00322.2014 http://scihub22266oqcxt.onion/10.1152/ajpcell.00322.2014 C4451352!4451352!25810260     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25810260&cmd=llinks): Failed to open stream: HTTP request failed! 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PPAR? inhibition modulates multiple reprogrammed metabolic pathways in kidney cancer and attenuates tumor growth |pdf=|usr=}}{{25810260}} gab.com Text PPAR inhibition modulates multiple reprogrammed metabolic pathways in kidney cancer and attenuates tumor growth JO: Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25810260 #FOAvip Kidney cancer [renal cell carcinoma (RCC)] is the sixth-most-common cancer in the United States, and its incidence is increasing. The current progression-free survival for patients with advanced RCC rarely extends beyond 1?2 yr due to the development of therapeutic resistance. We previously identified peroxisome proliferator-activating receptor-? (PPAR?) as a potential therapeutic target for this disease and showed that a specific PPAR? antagonist, GW6471, induced apoptosis and cell cycle arrest at G0/G1 in RCC cell lines associated with attenuation of cell cycle regulatory proteins. We now extend that work and show that PPAR? inhibition attenuates components of RCC metabolic reprogramming, capitalizing on the Warburg effect. The specific PPAR? inhibitor GW6471, as well as a siRNA specific to PPAR?, attenuates the enhanced fatty acid oxidation and oxidative phosphorylation associated with glycolysis inhibition, and PPAR? antagonism also blocks the enhanced glycolysis that has been observed in RCC cells; this effect did not occur in normal human kidney epithelial cells. Such cell type-specific inhibition of glycolysis corresponds with changes in protein levels of the oncogene c-Myc and has promising clinical implications. Furthermore, we show that treatment with GW6471 results in RCC tumor growth attenuation in a xenograft mouse model, with minimal obvious toxicity, a finding associated with the expected on-target effects on c-Myc. These studies demonstrate that several pivotal cancer-relevant metabolic pathways are inhibited by PPAR? antagonism. Our data support the concept that targeting PPAR?, with or without concurrent inhibition of glycolysis, is a potential novel and effective therapeutic approach for RCC that targets metabolic reprogramming in this tumor. Twit Text FOAVip PPAR inhibition modulates multiple reprogrammed metabolic pathways in kidney cancer and attenuates tumor growth ????Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25810260 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25810260 #FOAvip English Wikipedia <ref>{{Cite pmid|25810260}}</ref> PPAR? inhibition modulates multiple reprogrammed metabolic pathways in kidney cancer and attenuates tumor growth #MMPMID25810260 Abu Aboud O; Donohoe D; Bultman S; Fitch M; Riiff T; Hellerstein M; Weiss RH Am J Physiol Cell Physiol 2015[Jun]; 308 (11): C890-8 PMID25810260show ga Kidney cancer [renal cell carcinoma (RCC)] is the sixth-most-common cancer in the United States, and its incidence is increasing. The current progression-free survival for patients with advanced RCC rarely extends beyond 1?2 yr due to the development of therapeutic resistance. We previously identified peroxisome proliferator-activating receptor-? (PPAR?) as a potential therapeutic target for this disease and showed that a specific PPAR? antagonist, GW6471, induced apoptosis and cell cycle arrest at G0/G1 in RCC cell lines associated with attenuation of cell cycle regulatory proteins. We now extend that work and show that PPAR? inhibition attenuates components of RCC metabolic reprogramming, capitalizing on the Warburg effect. The specific PPAR? inhibitor GW6471, as well as a siRNA specific to PPAR?, attenuates the enhanced fatty acid oxidation and oxidative phosphorylation associated with glycolysis inhibition, and PPAR? antagonism also blocks the enhanced glycolysis that has been observed in RCC cells; this effect did not occur in normal human kidney epithelial cells. Such cell type-specific inhibition of glycolysis corresponds with changes in protein levels of the oncogene c-Myc and has promising clinical implications. Furthermore, we show that treatment with GW6471 results in RCC tumor growth attenuation in a xenograft mouse model, with minimal obvious toxicity, a finding associated with the expected on-target effects on c-Myc. These studies demonstrate that several pivotal cancer-relevant metabolic pathways are inhibited by PPAR? antagonism. Our data support the concept that targeting PPAR?, with or without concurrent inhibition of glycolysis, is a potential novel and effective therapeutic approach for RCC that targets metabolic reprogramming in this tumor. äPPAR? inhibition modulates multiple reprogrammed metabolic pathways in(epmc).pdf DeepDyve Pubget Overpricing