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10.1038/ni.3313 http://scihub22266oqcxt.onion/10.1038/ni.3313 C4684796!4684796!26523864     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Immunol 2016 ; 17 (1): 95-103 Nephropedia Template TP {{tp|p=26523864|t=2016. Cancer mediates effector T cell dysfunction by targeting microRNAs and EZH2 via glycolysis restriction |pdf=|usr=}}{{26523864}} gab.com Text Cancer mediates effector T cell dysfunction by targeting microRNAs and EZH2 via glycolysis restriction JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26523864 #FOAvip Aerobic glycolysis regulates T cell function. However, if and how primary cancer alters T cell glycolytic metabolism and affects tumor immunity remains a question in cancer patients. Here we report that ovarian cancers imposed glucose restriction on T cells and dampened their function via maintaining high expression of microRNA101 and microRNA26a, which constrained expression of the methyltransferase EZH2. EZH2 activated the Notch pathway by suppressing Notch repressors, Numb and Fbxw7, via H3K27me3, and consequently stimulated T cell polyfunctional cytokine expression and promoted their survival via Bcl-2 signaling. Moreover, human shRNA-knockdown-EZH2-deficient T cells elicited poor anti-tumor immunity. EZH2+CD8+ T cells were associated with improved cancer patient survival. Together, the data unveil a novel metabolic target and mechanism of cancer immune evasion. Twit Text FOAVip Cancer mediates effector T cell dysfunction by targeting microRNAs and EZH2 via glycolysis restriction ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26523864 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26523864 #FOAvip English Wikipedia <ref>{{Cite pmid|26523864}}</ref> Cancer mediates effector T cell dysfunction by targeting microRNAs and EZH2 via glycolysis restriction #MMPMID26523864 Zhao E; Maj T; Kryczek I; Li W; Wu K; Zhao L; Wei S; Crespo J; Wan S; Vatan L; Szeliga W; Shao I; Wang Y; Liu Y; Varambally S; Chinnaiyan AM; Welling TH; Marquez VE; Kotarski J; Wang H; Wang Z; Zhang Y; Liu R; Wang G; Zou W Nat Immunol 2016[Jan]; 17 (1): 95-103 PMID26523864show ga Aerobic glycolysis regulates T cell function. However, if and how primary cancer alters T cell glycolytic metabolism and affects tumor immunity remains a question in cancer patients. Here we report that ovarian cancers imposed glucose restriction on T cells and dampened their function via maintaining high expression of microRNA101 and microRNA26a, which constrained expression of the methyltransferase EZH2. EZH2 activated the Notch pathway by suppressing Notch repressors, Numb and Fbxw7, via H3K27me3, and consequently stimulated T cell polyfunctional cytokine expression and promoted their survival via Bcl-2 signaling. Moreover, human shRNA-knockdown-EZH2-deficient T cells elicited poor anti-tumor immunity. EZH2+CD8+ T cells were associated with improved cancer patient survival. Together, the data unveil a novel metabolic target and mechanism of cancer immune evasion. äCancer mediates effector T cell dysfunction by targeting microRNAs and(epmc).pdf DeepDyve Pubget Overpricing