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10.18632/oncotarget.13860 http://scihub22266oqcxt.onion/10.18632/oncotarget.13860 C5352374!5352374!27974704     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27974704&cmd=llinks): Failed to open stream: HTTP request failed! 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MED15 overexpression in prostate cancer arises during androgen deprivation therapy via PI3K/mTOR signaling |pdf=|usr=}}{{27974704}} gab.com Text MED15 overexpression in prostate cancer arises during androgen deprivation therapy via PI3K/mTOR signaling JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27974704 #FOAvip Androgen deprivation therapy (ADT) is the main therapeutic option for advanced prostate cancer (PCa). After initial regression, most tumors develop into castration-resistant PCa (CRPC). Previously, we found the Mediator complex subunit MED15 to be overexpressed in CRPC and to correlate with clinical outcome. Therefore, we investigated whether MED15 is implicated in the signaling changes taking place during progression to CRPC. Immunohistochemistry (IHC) for MED15 on matched samples from the same patients before and after ADT reveals significantly increased MED15 expression after ADT in 72%. A validation cohort comprising samples before and after therapy confirmed our observations. Protein analysis for pAKT and pSMAD3 shows that MED15 correlates with PI3K and TGFß activities, respectively, and that hyper-activation of both pathways simultaneously correlates with highest levels of MED15. We further show that MED15 protein expression increases in LNCaP cells under androgen deprivation, and via EGF mediated PI3K activation. PI3K/mTOR and TGFß-receptor inhibition results in decreased MED15 expression. MED15 knockdown reduces LNCaP cell viability and induces apoptosis during androgen deprivation, while cell cycle is not affected. Collectively, MED15 overexpression arises during ADT via hyper-activation of PI3K/mTOR signaling, thus MED15 may serve as a predictive marker for response to PI3K/mTOR inhibitors. Furthermore, MED15 is potentially a therapeutic target for the treatment of CRPC. Twit Text FOAVip MED15 overexpression in prostate cancer arises during androgen deprivation therapy via PI3K/mTOR signaling ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27974704 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27974704 #FOAvip English Wikipedia <ref>{{Cite pmid|27974704}}</ref> MED15 overexpression in prostate cancer arises during androgen deprivation therapy via PI3K/mTOR signaling #MMPMID27974704 Offermann A; Vlasic I; Syring I; Vogel W; Ruiz C; Zellweger T; Rentsch CA; Hagedorn S; Behrends J; Nowak M; Merseburger A; Bubendorf L; Kirfel J; Duensing S; Adler D; Perner S Oncotarget 2017[Jan]; 8 (5): 7964-76 PMID27974704show ga Androgen deprivation therapy (ADT) is the main therapeutic option for advanced prostate cancer (PCa). After initial regression, most tumors develop into castration-resistant PCa (CRPC). Previously, we found the Mediator complex subunit MED15 to be overexpressed in CRPC and to correlate with clinical outcome. Therefore, we investigated whether MED15 is implicated in the signaling changes taking place during progression to CRPC. Immunohistochemistry (IHC) for MED15 on matched samples from the same patients before and after ADT reveals significantly increased MED15 expression after ADT in 72%. A validation cohort comprising samples before and after therapy confirmed our observations. Protein analysis for pAKT and pSMAD3 shows that MED15 correlates with PI3K and TGFß activities, respectively, and that hyper-activation of both pathways simultaneously correlates with highest levels of MED15. We further show that MED15 protein expression increases in LNCaP cells under androgen deprivation, and via EGF mediated PI3K activation. PI3K/mTOR and TGFß-receptor inhibition results in decreased MED15 expression. MED15 knockdown reduces LNCaP cell viability and induces apoptosis during androgen deprivation, while cell cycle is not affected. Collectively, MED15 overexpression arises during ADT via hyper-activation of PI3K/mTOR signaling, thus MED15 may serve as a predictive marker for response to PI3K/mTOR inhibitors. Furthermore, MED15 is potentially a therapeutic target for the treatment of CRPC. äMED15 overexpression in prostate cancer arises during androgen depriva(epmc).pdf DeepDyve Pubget Overpricing