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10.1158/0008-5472.CAN-15-1524 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-15-1524 C5031238!5031238 !27197188     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27197188 &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       Cancer+Res 2016 ; 76 (13 ): 3884-94 Nephropedia Template TP {{tp|p=27197188 |t=2016. Renalase Expression by Melanoma and Tumor-Associated Macrophages Promotes Tumor Growth through a STAT3-Mediated Mechanism |pdf=|usr=}}{{27197188 }} gab.com Text Renalase Expression by Melanoma and Tumor-Associated Macrophages Promotes Tumor Growth through a STAT3-Mediated Mechanism JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27197188 #FOAvip To sustain their proliferation, cancer cells overcome negative-acting signals that restrain their growth and promote senescence and cell death. Renalase (RNLS) is a secreted flavoprotein that functions as a survival factor after ischemic and toxic injury, signaling through the plasma calcium channel PMCA4b to activate the PI3K/AKT and MAPK pathways. We show that RNLS expression is increased markedly in primary melanomas and CD163(+) tumor-associated macrophages (TAM). In clinical specimens, RNLS expression in the tumor correlated inversely with disease-specific survival, suggesting a pathogenic role for RNLS. Attenuation of RNLS by RNAi, blocking antibodies, or an RNLS-derived inhibitory peptide decreased melanoma cell survival, and anti-RNLS therapy blocked tumor growth in vivo in murine xenograft assays. Mechanistic investigations showed that increased apoptosis in tumor cells was temporally related to p38 MAPK-mediated Bax activation and that increased cell growth arrest was associated with elevated expression of the cell-cycle inhibitor p21. Overall, our results established a role for the secreted flavoprotein RNLS in promoting melanoma cell growth and CD163(+) TAM in the tumor microenvironment, with potential therapeutic implications for the management of melanoma. Cancer Res; 76(13); 3884-94. ©2016 AACR. Twit Text FOAVip Renalase Expression by Melanoma and Tumor-Associated Macrophages Promotes Tumor Growth through a STAT3-Mediated Mechanism ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27197188 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27197188 #FOAvip English Wikipedia <ref>{{Cite pmid|27197188 }}</ref> Renalase Expression by Melanoma and Tumor-Associated Macrophages Promotes Tumor Growth through a STAT3-Mediated Mechanism #MMPMID27197188 Hollander L ; Guo X ; Velazquez H ; Chang J ; Safirstein R ; Kluger H ; Cha C ; Desir GV Cancer Res 2016[Jul]; 76 (13 ): 3884-94 PMID27197188 show ga To sustain their proliferation, cancer cells overcome negative-acting signals that restrain their growth and promote senescence and cell death. Renalase (RNLS) is a secreted flavoprotein that functions as a survival factor after ischemic and toxic injury, signaling through the plasma calcium channel PMCA4b to activate the PI3K/AKT and MAPK pathways. We show that RNLS expression is increased markedly in primary melanomas and CD163(+) tumor-associated macrophages (TAM). In clinical specimens, RNLS expression in the tumor correlated inversely with disease-specific survival, suggesting a pathogenic role for RNLS. Attenuation of RNLS by RNAi, blocking antibodies, or an RNLS-derived inhibitory peptide decreased melanoma cell survival, and anti-RNLS therapy blocked tumor growth in vivo in murine xenograft assays. Mechanistic investigations showed that increased apoptosis in tumor cells was temporally related to p38 MAPK-mediated Bax activation and that increased cell growth arrest was associated with elevated expression of the cell-cycle inhibitor p21. Overall, our results established a role for the secreted flavoprotein RNLS in promoting melanoma cell growth and CD163(+) TAM in the tumor microenvironment, with potential therapeutic implications for the management of melanoma. Cancer Res; 76(13); 3884-94. ©2016 AACR. |*Gene Expression Regulation, Neoplastic [MESH] |Animals [MESH] |Apoptosis [MESH] |Biomarkers, Tumor/*metabolism [MESH] |Blotting, Western [MESH] |Case-Control Studies [MESH] |Cell Cycle [MESH] |Cell Proliferation [MESH] |Female [MESH] |Follow-Up Studies [MESH] |Humans [MESH] |Immunoenzyme Techniques [MESH] |Macrophages/metabolism/*pathology [MESH] |Male [MESH] |Melanoma/metabolism/*pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Nude [MESH] |Monoamine Oxidase/*metabolism [MESH] |Neoplasm Staging [MESH] |Prognosis [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |STAT3 Transcription Factor/*metabolism [MESH] |Signal Transduction [MESH] |Survival Rate [MESH] |Tumor Cells, Cultured [MESH] |Xenograft Model Antitumor Assays [MESH]Renalase Expression by Melanoma and Tumor-Associated Macrophages Promo(epmc).pdf DeepDyve Pubget Overpricing