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10.1172/JCI86505 http://scihub22266oqcxt.onion/10.1172/JCI86505 C5127674!5127674!27820701     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27820701&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest ä ; 126 (12): 4585-602 Nephropedia Template TP {{tp|p=27820701|t=ä. MicroRNA-424 impairs ubiquitination to activate STAT3 and promote prostate tumor progression |pdf=|usr=}}{{27820701}} gab.com Text MicroRNA-424 impairs ubiquitination to activate STAT3 and promote prostate tumor progression JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27820701 #FOAvip Mutations and deletions in components of ubiquitin ligase complexes that lead to alterations in protein turnover are important mechanisms in driving tumorigenesis. Here we describe an alternative mechanism involving upregulation of the microRNA miR-424 that leads to impaired ubiquitination and degradation of oncogenic transcription factors in prostate cancers. We found that miR-424 targets the E3 ubiquitin ligase COP1 and identified STAT3 as a key substrate of COP1 in promoting tumorigenic and cancer stem-like properties in prostate epithelial cells. Altered protein turnover due to impaired COP1 function led to accumulation and enhanced basal and cytokine-induced activity of STAT3. We further determined that loss of the ETS factor ESE3/EHF is the initial event that triggers the deregulation of the miR-424/COP1/STAT3 axis. COP1 silencing and STAT3 activation were effectively reverted by blocking of miR-424, suggesting a possible strategy to attack this key node of tumorigenesis in ESE3/EHF?deficient tumors. These results establish miR-424 as an oncogenic effector linked to noncanonical activation of STAT3 and as a potential therapeutic target. Twit Text FOAVip MicroRNA-424 impairs ubiquitination to activate STAT3 and promote prostate tumor progression ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27820701 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27820701 #FOAvip English Wikipedia <ref>{{Cite pmid|27820701}}</ref> MicroRNA-424 impairs ubiquitination to activate STAT3 and promote prostate tumor progression #MMPMID27820701 Dallavalle C; Albino D; Civenni G; Merulla J; Ostano P; Mello-Grand M; Rossi S; Losa M; D?Ambrosio G; Sessa F; Thalmann GN; Garcia-Escudero R; Zitella A; Chiorino G; Catapano CV; Carbone GM J Clin Invest ä[]; 126 (12): 4585-602 PMID27820701show ga Mutations and deletions in components of ubiquitin ligase complexes that lead to alterations in protein turnover are important mechanisms in driving tumorigenesis. Here we describe an alternative mechanism involving upregulation of the microRNA miR-424 that leads to impaired ubiquitination and degradation of oncogenic transcription factors in prostate cancers. We found that miR-424 targets the E3 ubiquitin ligase COP1 and identified STAT3 as a key substrate of COP1 in promoting tumorigenic and cancer stem-like properties in prostate epithelial cells. Altered protein turnover due to impaired COP1 function led to accumulation and enhanced basal and cytokine-induced activity of STAT3. We further determined that loss of the ETS factor ESE3/EHF is the initial event that triggers the deregulation of the miR-424/COP1/STAT3 axis. COP1 silencing and STAT3 activation were effectively reverted by blocking of miR-424, suggesting a possible strategy to attack this key node of tumorigenesis in ESE3/EHF?deficient tumors. These results establish miR-424 as an oncogenic effector linked to noncanonical activation of STAT3 and as a potential therapeutic target. äMicroRNA-424 impairs ubiquitination to activate STAT3 and promote pros(epmc).pdf DeepDyve Pubget Overpricing