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10.1016/j.chembiol.2016.03.017 http://scihub22266oqcxt.onion/10.1016/j.chembiol.2016.03.017 C4876719!4876719!27185638     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Chem+Biol 2016 ; 23 (5): 567-78 Nephropedia Template TP {{tp|p=27185638|t=2016. GSTP1 is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity |pdf=|usr=}}{{27185638}} gab.com Text GSTP1 is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity JO: Cell Chem Biol http://www.kidney.de/pget.php?&tw=1&pmid=27185638 #FOAvip Breast cancers possess fundamentally altered metabolism that fuels their pathogenicity. While many metabolic drivers of breast cancers have been identified, the metabolic pathways that mediate breast cancer malignancy and poor prognosis are less well understood. Here, we used a reactivity-based chemoproteomic platform to profile metabolic enzymes that are enriched in breast cancer cell-types linked to poor prognosis, including triple-negative breast cancer (TNBC) cells and breast cancer cells that have undergone an epithelial-mesenchymal transition-like state of heightened malignancy. We identified glutathione-S-transferase Pi 1 (GSTP1) as a novel TNBC target that controls cancer pathogenicity by regulating glycolytic and lipid metabolism, energetics, and oncogenic signaling pathways through a protein interaction that activates glyceraldehyde-3-phosphate dehydrogenase activity. We show that genetic or pharmacological inactivation of GSTP1 impairs cell survival and tumorigenesis in TNBC cells. We put forth GSTP1 inhibitors as a novel therapeutic strategy for combatting TNBCs through impairing key cancer metabolism and signaling pathways. Twit Text FOAVip GSTP1 is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity ????Cell Chem Biol http://www.kidney.de/pget.php?&tw=1&pmid=27185638 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27185638 #FOAvip English Wikipedia <ref>{{Cite pmid|27185638}}</ref> GSTP1 is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity #MMPMID27185638 Louie SM; Grossman EA; Crawford LA; Ding L; Camarda R; Huffman TR; Miyamoto DK; Goga A; Weerapana E; Nomura DK Cell Chem Biol 2016[May]; 23 (5): 567-78 PMID27185638show ga Breast cancers possess fundamentally altered metabolism that fuels their pathogenicity. While many metabolic drivers of breast cancers have been identified, the metabolic pathways that mediate breast cancer malignancy and poor prognosis are less well understood. Here, we used a reactivity-based chemoproteomic platform to profile metabolic enzymes that are enriched in breast cancer cell-types linked to poor prognosis, including triple-negative breast cancer (TNBC) cells and breast cancer cells that have undergone an epithelial-mesenchymal transition-like state of heightened malignancy. We identified glutathione-S-transferase Pi 1 (GSTP1) as a novel TNBC target that controls cancer pathogenicity by regulating glycolytic and lipid metabolism, energetics, and oncogenic signaling pathways through a protein interaction that activates glyceraldehyde-3-phosphate dehydrogenase activity. We show that genetic or pharmacological inactivation of GSTP1 impairs cell survival and tumorigenesis in TNBC cells. We put forth GSTP1 inhibitors as a novel therapeutic strategy for combatting TNBCs through impairing key cancer metabolism and signaling pathways. äGSTP1 is a Driver of Triple-Negative Breast Cancer Cell Metabolism and(epmc).pdf DeepDyve Pubget Overpricing