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10.18632/oncotarget.3709 http://scihub22266oqcxt.onion/10.18632/oncotarget.3709 C4558173!4558173 !25909225     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25909225 &cmd=llinks): Failed to open stream: HTTP request failed! 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PBK/TOPK enhances aggressive phenotype in prostate cancer via ?-catenin-TCF/LEF-mediated matrix metalloproteinases production and invasion |pdf=|usr=}}{{25909225 }} gab.com Text PBK/TOPK enhances aggressive phenotype in prostate cancer via -catenin-TCF/LEF-mediated matrix metalloproteinases production and invasion JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25909225 #FOAvip A current challenge in prostate cancer treatment is how to differentiate aggressive disease from indolent prostate cancer. There is an urgent need to identify markers that would accurately distinguish indolent prostate cancer from aggressive disease. The aim of this study was to evaluate the role of PDZ Domain-binding kinase (PBK) in prostate cancer and to determine if PBK expression enhances aggressiveness in prostate cancer. Using archival tissue samples, gain-of-function and loss-of-function studies, we show that PBK expression is up-regulated in prostate cancer, and its expression level is commensurate with invasiveness. Modulation of PBK expression and function causally regulates the invasive ability of prostate cancer cells. Production of matrix metalloproteinases-2 and -9, which are key players in metastatic invasion, is up-regulated, and the promoters of these genes are transcriptionally activated by PBK via increased ?-catenin-TCF/LEF signaling. Prostate cancer tissue specimens show that PBK's expression correlates with aggressive disease and distant metastasis in bone, lymph node and abdomen. Our in vitro and in situ data are in agreement that PBK could be a prognostic biomarker for prostate cancer that would discriminate aggressive prostate cancer from indolent disease, and is a potential target for the therapeutic intervention of aggressive prostate cancer in men. Twit Text FOAVip PBK/TOPK enhances aggressive phenotype in prostate cancer via -catenin-TCF/LEF-mediated matrix metalloproteinases production and invasion ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25909225 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25909225 #FOAvip English Wikipedia <ref>{{Cite pmid|25909225 }}</ref> PBK/TOPK enhances aggressive phenotype in prostate cancer via ?-catenin-TCF/LEF-mediated matrix metalloproteinases production and invasion #MMPMID25909225 Brown-Clay JD ; Shenoy DN ; Timofeeva O ; Kallakury BV ; Nandi AK ; Banerjee PP Oncotarget 2015[Jun]; 6 (17 ): 15594-609 PMID25909225 show ga A current challenge in prostate cancer treatment is how to differentiate aggressive disease from indolent prostate cancer. There is an urgent need to identify markers that would accurately distinguish indolent prostate cancer from aggressive disease. The aim of this study was to evaluate the role of PDZ Domain-binding kinase (PBK) in prostate cancer and to determine if PBK expression enhances aggressiveness in prostate cancer. Using archival tissue samples, gain-of-function and loss-of-function studies, we show that PBK expression is up-regulated in prostate cancer, and its expression level is commensurate with invasiveness. Modulation of PBK expression and function causally regulates the invasive ability of prostate cancer cells. Production of matrix metalloproteinases-2 and -9, which are key players in metastatic invasion, is up-regulated, and the promoters of these genes are transcriptionally activated by PBK via increased ?-catenin-TCF/LEF signaling. Prostate cancer tissue specimens show that PBK's expression correlates with aggressive disease and distant metastasis in bone, lymph node and abdomen. Our in vitro and in situ data are in agreement that PBK could be a prognostic biomarker for prostate cancer that would discriminate aggressive prostate cancer from indolent disease, and is a potential target for the therapeutic intervention of aggressive prostate cancer in men. |Abdominal Neoplasms/secondary [MESH] |Biomarkers, Tumor/genetics/*metabolism [MESH] |Bone Neoplasms/secondary [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Humans [MESH] |Lymphatic Metastasis/pathology [MESH] |Male [MESH] |Matrix Metalloproteinase 2/biosynthesis/genetics [MESH] |Matrix Metalloproteinase 9/biosynthesis/genetics [MESH] |Mitogen-Activated Protein Kinase Kinases/genetics/*metabolism [MESH] |Neoplasm Invasiveness [MESH] |Promoter Regions, Genetic/genetics [MESH] |Prostatic Neoplasms/*pathology [MESH] |Signal Transduction [MESH] |TCF Transcription Factors/*metabolism [MESH]PBK/TOPK enhances aggressive phenotype in prostate cancer via ?-cate(epmc).pdf DeepDyve Pubget Overpricing