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10.1038/ncomms8736 http://scihub22266oqcxt.onion/10.1038/ncomms8736 C4525303!4525303!26198641     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2015 ; 6 (ä): ä Nephropedia Template TP {{tp|p=26198641|t=2015. STAT3 regulated ARF expression suppresses prostate cancer metastasis |pdf=|usr=}}{{26198641}} gab.com Text STAT3 regulated ARF expression suppresses prostate cancer metastasis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26198641 #FOAvip Prostate cancer (PCa) is the most prevalent cancer in men. Hyperactive STAT3 is thought to be oncogenic in PCa. However, targeting of the IL-6/STAT3 axis in PCa patients has failed to provide therapeutic benefit. Here we show that genetic inactivation of Stat3 or IL-6 signalling in a Pten-deficient PCa mouse model accelerates cancer progression leading to metastasis. Mechanistically, we identify p19ARF as a direct Stat3 target. Loss of Stat3 signalling disrupts the ARF?Mdm2?p53 tumour suppressor axis bypassing senescence. Strikingly, we also identify STAT3 and CDKN2A mutations in primary human PCa. STAT3 and CDKN2A deletions co-occurred with high frequency in PCa metastases. In accordance, loss of STAT3 and p14ARF expression in patient tumours correlates with increased risk of disease recurrence and metastatic PCa. Thus, STAT3 and ARF may be prognostic markers to stratify high from low risk PCa patients. Our findings challenge the current discussion on therapeutic benefit or risk of IL-6/STAT3 inhibition. Twit Text FOAVip STAT3 regulated ARF expression suppresses prostate cancer metastasis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26198641 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26198641 #FOAvip English Wikipedia <ref>{{Cite pmid|26198641}}</ref> STAT3 regulated ARF expression suppresses prostate cancer metastasis #MMPMID26198641 Pencik J; Schlederer M; Gruber W; Unger C; Walker SM; Chalaris A; Marié IJ; Hassler MR; Javaheri T; Aksoy O; Blayney JK; Prutsch N; Skucha A; Herac M; Krämer OH; Mazal P; Grebien F; Egger G; Poli V; Mikulits W; Eferl R; Esterbauer H; Kennedy R; Fend F; Scharpf M; Braun M; Perner S; Levy DE; Malcolm T; Turner SD; Haitel A; Susani M; Moazzami A; Rose-John S; Aberger F; Merkel O; Moriggl R; Culig Z; Dolznig H; Kenner L Nat Commun 2015[]; 6 (ä): ä PMID26198641show ga Prostate cancer (PCa) is the most prevalent cancer in men. Hyperactive STAT3 is thought to be oncogenic in PCa. However, targeting of the IL-6/STAT3 axis in PCa patients has failed to provide therapeutic benefit. Here we show that genetic inactivation of Stat3 or IL-6 signalling in a Pten-deficient PCa mouse model accelerates cancer progression leading to metastasis. Mechanistically, we identify p19ARF as a direct Stat3 target. Loss of Stat3 signalling disrupts the ARF?Mdm2?p53 tumour suppressor axis bypassing senescence. Strikingly, we also identify STAT3 and CDKN2A mutations in primary human PCa. STAT3 and CDKN2A deletions co-occurred with high frequency in PCa metastases. In accordance, loss of STAT3 and p14ARF expression in patient tumours correlates with increased risk of disease recurrence and metastatic PCa. Thus, STAT3 and ARF may be prognostic markers to stratify high from low risk PCa patients. Our findings challenge the current discussion on therapeutic benefit or risk of IL-6/STAT3 inhibition. äSTAT3 regulated ARF expression suppresses prostate cancer metastasis (epmc).pdf DeepDyve Pubget Overpricing