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10.1158/0008-5472.CAN-14-0476 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-14-0476 C4209379!4209379 !25274033     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25274033 &cmd=llinks): Failed to open stream: HTTP request failed! 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Androgen receptor is the key transcriptional mediator of the tumor suppressor SPOP in prostate cancer |pdf=|usr=}}{{25274033 }} gab.com Text Androgen receptor is the key transcriptional mediator of the tumor suppressor SPOP in prostate cancer JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25274033 #FOAvip Somatic missense mutations in the substrate-binding pocket of the E3 ubiquitin ligase adaptor SPOP are present in up to 15% of human prostate adenocarcinomas, but are rare in other malignancies, suggesting a prostate-specific mechanism of action. SPOP promotes ubiquitination and degradation of several protein substrates, including the androgen receptor (AR) coactivator SRC-3. However, the relative contributions that SPOP substrates may make to the pathophysiology of SPOP-mutant (mt) prostate adenocarcinomas are unknown. Using an unbiased bioinformatics approach, we determined that the gene expression profile of prostate adenocarcinoma cells engineered to express mt-SPOP overlaps greatly with the gene signature of both SRC-3 and AR transcriptional output, with a stronger similarity to AR than SRC-3. This finding suggests that in addition to its SRC-3-mediated effects, SPOP also exerts SRC-3-independent effects that are AR-mediated. Indeed, we found that wild-type (wt) but not prostate adenocarcinoma-associated mutants of SPOP promoted AR ubiquitination and degradation, acting directly through a SPOP-binding motif in the hinge region of AR. In support of these results, tumor xenografts composed of prostate adenocarcinoma cells expressing mt-SPOP exhibited higher AR protein levels and grew faster than tumors composed of prostate adenocarcinoma cells expressing wt-SPOP. Furthermore, genetic ablation of SPOP was sufficient to increase AR protein levels in mouse prostate. Examination of public human prostate adenocarcinoma datasets confirmed a strong link between transcriptomic profiles of mt-SPOP and AR. Overall, our studies highlight the AR axis as the key transcriptional output of SPOP in prostate adenocarcinoma and provide an explanation for the prostate-specific tumor suppressor role of wt-SPOP. Twit Text FOAVip Androgen receptor is the key transcriptional mediator of the tumor suppressor SPOP in prostate cancer ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25274033 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25274033 #FOAvip English Wikipedia <ref>{{Cite pmid|25274033 }}</ref> Androgen receptor is the key transcriptional mediator of the tumor suppressor SPOP in prostate cancer #MMPMID25274033 Geng C ; Rajapakshe K ; Shah SS ; Shou J ; Eedunuri VK ; Foley C ; Fiskus W ; Rajendran M ; Chew SA ; Zimmermann M ; Bond R ; He B ; Coarfa C ; Mitsiades N Cancer Res 2014[Oct]; 74 (19 ): 5631-43 PMID25274033 show ga Somatic missense mutations in the substrate-binding pocket of the E3 ubiquitin ligase adaptor SPOP are present in up to 15% of human prostate adenocarcinomas, but are rare in other malignancies, suggesting a prostate-specific mechanism of action. SPOP promotes ubiquitination and degradation of several protein substrates, including the androgen receptor (AR) coactivator SRC-3. However, the relative contributions that SPOP substrates may make to the pathophysiology of SPOP-mutant (mt) prostate adenocarcinomas are unknown. Using an unbiased bioinformatics approach, we determined that the gene expression profile of prostate adenocarcinoma cells engineered to express mt-SPOP overlaps greatly with the gene signature of both SRC-3 and AR transcriptional output, with a stronger similarity to AR than SRC-3. This finding suggests that in addition to its SRC-3-mediated effects, SPOP also exerts SRC-3-independent effects that are AR-mediated. Indeed, we found that wild-type (wt) but not prostate adenocarcinoma-associated mutants of SPOP promoted AR ubiquitination and degradation, acting directly through a SPOP-binding motif in the hinge region of AR. In support of these results, tumor xenografts composed of prostate adenocarcinoma cells expressing mt-SPOP exhibited higher AR protein levels and grew faster than tumors composed of prostate adenocarcinoma cells expressing wt-SPOP. Furthermore, genetic ablation of SPOP was sufficient to increase AR protein levels in mouse prostate. Examination of public human prostate adenocarcinoma datasets confirmed a strong link between transcriptomic profiles of mt-SPOP and AR. Overall, our studies highlight the AR axis as the key transcriptional output of SPOP in prostate adenocarcinoma and provide an explanation for the prostate-specific tumor suppressor role of wt-SPOP. |*Genes, Tumor Suppressor [MESH] |Adenocarcinoma/genetics/*physiopathology [MESH] |Androgens/physiology [MESH] |Gene Expression Profiling [MESH] |Humans [MESH] |Male [MESH] |Mutation [MESH] |Nuclear Proteins/*genetics [MESH] |Nuclear Receptor Coactivator 3/physiology [MESH] |Prostatic Neoplasms/genetics/*physiopathology [MESH] |Receptors, Androgen/*physiology [MESH] |Repressor Proteins/*genetics [MESH]Androgen receptor is the key transcriptional mediator of the tumor sup(epmc).pdf DeepDyve Pubget Overpricing