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10.1128/MCB.00825-15 http://scihub22266oqcxt.onion/10.1128/MCB.00825-15 C4648817!4648817 !26438599     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26438599 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cotargeting Polo-Like Kinase 1 and the Wnt/?-Catenin Signaling Pathway in Castration-Resistant Prostate Cancer |pdf=|usr=}}{{26438599 }} gab.com Text Cotargeting Polo-Like Kinase 1 and the Wnt/ -Catenin Signaling Pathway in Castration-Resistant Prostate Cancer JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26438599 #FOAvip The Wnt/?-catenin signaling pathway has been identified as one of the predominantly upregulated pathways in castration-resistant prostate cancer (CRPC). However, whether targeting the ?-catenin pathway will prove effective as a CRPC treatment remains unknown. Polo-like kinase 1 (Plk1) is a critical regulator in many cell cycle events, and its level is significantly elevated upon castration of mice carrying xenograft prostate tumors. Indeed, inhibition of Plk1 has been shown to inhibit tumor growth in several in vivo studies. Here, we show that Plk1 is a negative regulator of Wnt/?-catenin signaling. Plk1 inhibition or depletion enhances the level of cytosolic and nuclear ?-catenin in human prostate cancer cells. Furthermore, inhibition of Wnt/?-catenin signaling significantly potentiates the antineoplastic activity of the Plk1 inhibitor BI2536 in both cultured prostate cancer cells and CRPC xenograft tumors. Mechanistically, axin2, a negative regulator of the ?-catenin pathway, serves as a substrate of Plk1, and Plk1 phosphorylation of axin2 facilitates the degradation of ?-catenin by enhancing binding between glycogen synthase kinase 3? (GSK3?) and ?-catenin. Plk1-phosphorylated axin2 also exhibits resistance to Cdc20-mediated degradation. Overall, this study identifies a novel Plk1-Wnt signaling axis in prostate cancer, offering a promising new therapeutic option to treat CRPC. Twit Text FOAVip Cotargeting Polo-Like Kinase 1 and the Wnt/ -Catenin Signaling Pathway in Castration-Resistant Prostate Cancer ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26438599 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26438599 #FOAvip English Wikipedia <ref>{{Cite pmid|26438599 }}</ref> Cotargeting Polo-Like Kinase 1 and the Wnt/?-Catenin Signaling Pathway in Castration-Resistant Prostate Cancer #MMPMID26438599 Li J ; Karki A ; Hodges KB ; Ahmad N ; Zoubeidi A ; Strebhardt K ; Ratliff TL ; Konieczny SF ; Liu X Mol Cell Biol 2015[Dec]; 35 (24 ): 4185-98 PMID26438599 show ga The Wnt/?-catenin signaling pathway has been identified as one of the predominantly upregulated pathways in castration-resistant prostate cancer (CRPC). However, whether targeting the ?-catenin pathway will prove effective as a CRPC treatment remains unknown. Polo-like kinase 1 (Plk1) is a critical regulator in many cell cycle events, and its level is significantly elevated upon castration of mice carrying xenograft prostate tumors. Indeed, inhibition of Plk1 has been shown to inhibit tumor growth in several in vivo studies. Here, we show that Plk1 is a negative regulator of Wnt/?-catenin signaling. Plk1 inhibition or depletion enhances the level of cytosolic and nuclear ?-catenin in human prostate cancer cells. Furthermore, inhibition of Wnt/?-catenin signaling significantly potentiates the antineoplastic activity of the Plk1 inhibitor BI2536 in both cultured prostate cancer cells and CRPC xenograft tumors. Mechanistically, axin2, a negative regulator of the ?-catenin pathway, serves as a substrate of Plk1, and Plk1 phosphorylation of axin2 facilitates the degradation of ?-catenin by enhancing binding between glycogen synthase kinase 3? (GSK3?) and ?-catenin. Plk1-phosphorylated axin2 also exhibits resistance to Cdc20-mediated degradation. Overall, this study identifies a novel Plk1-Wnt signaling axis in prostate cancer, offering a promising new therapeutic option to treat CRPC. |Animals [MESH] |Antimitotic Agents/pharmacology [MESH] |Axin Protein/metabolism [MESH] |Cdc20 Proteins/metabolism [MESH] |Cell Cycle Proteins/antagonists & inhibitors/*metabolism [MESH] |Cell Line, Tumor [MESH] |Glycogen Synthase Kinase 3 beta [MESH] |Glycogen Synthase Kinase 3/metabolism [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Male [MESH] |Mice [MESH] |Neoplasm Transplantation [MESH] |Phosphorylation [MESH] |Polo-Like Kinase 1 [MESH] |Prostatic Neoplasms, Castration-Resistant/*drug therapy/pathology [MESH] |Protein Serine-Threonine Kinases/antagonists & inhibitors/*metabolism [MESH] |Proto-Oncogene Proteins/antagonists & inhibitors/*metabolism [MESH] |Pteridines/pharmacology [MESH] |Transplantation, Heterologous [MESH] |Wnt Proteins/antagonists & inhibitors/*metabolism [MESH] |Wnt Signaling Pathway/*drug effects [MESH]Cotargeting Polo-Like Kinase 1 and the Wnt/?-Catenin Signaling Pathway(epmc).pdf DeepDyve Pubget Overpricing