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10.1016/j.neo.2017.01.004 http://scihub22266oqcxt.onion/10.1016/j.neo.2017.01.004 C5345960!5345960 !28284058     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28284058 &cmd=llinks): Failed to open stream: HTTP request failed! 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The Transient Receptor Potential Melastatin 7 Channel Regulates Pancreatic Cancer Cell Invasion through the Hsp90?/uPA/MMP2 pathway |pdf=|usr=}}{{28284058 }} gab.com Text The Transient Receptor Potential Melastatin 7 Channel Regulates Pancreatic Cancer Cell Invasion through the Hsp90 /uPA/MMP2 pathway JO: Neoplasia http://www.kidney.de/pget.php?&tw=1&pmid=28284058 #FOAvip Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a very poor prognosis. There is an urgent need to better understand the molecular mechanisms that regulate PDAC cell aggressiveness. The transient receptor potential melastatin 7 (TRPM7) is a nonselective cationic channel that mainly conducts Ca(2+) and Mg(2+). TRPM7 is overexpressed in numerous malignancies including PDAC. In the present study, we used the PANC-1 and MIA PaCa-2 cell lines to specifically assess the role of TRPM7 in cell invasion and matrix metalloproteinase secretion. We show that TRPM7 regulates Mg(2+) homeostasis and constitutive cation entry in both PDAC cell lines. Moreover, cell invasion is strongly reduced by TRPM7 silencing without affecting the cell viability. Conditioned media were further studied, by gel zymography, to detect matrix metalloproteinase (MMP) secretion in PDAC cells. Our results show that MMP-2, urokinase plasminogen activator (uPA), and heat-shock protein 90? (Hsp90?) secretions are significantly decreased in TRPM7-deficient PDAC cells. Moreover, TRPM7 expression in human PDAC lymph node metastasis is correlated to the channel expression in primary tumor. Taken together, our results show that TRPM7 is involved in PDAC cell invasion through regulation of Hsp90?/uPA/MMP-2 proteolytic axis, confirming that this channel could be a promising biomarker and possibly a target for PDAC metastasis therapy. Twit Text FOAVip The Transient Receptor Potential Melastatin 7 Channel Regulates Pancreatic Cancer Cell Invasion through the Hsp90 /uPA/MMP2 pathway ????Neoplasia http://www.kidney.de/pget.php?&tw=1&pmid=28284058 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28284058 #FOAvip English Wikipedia <ref>{{Cite pmid|28284058 }}</ref> The Transient Receptor Potential Melastatin 7 Channel Regulates Pancreatic Cancer Cell Invasion through the Hsp90?/uPA/MMP2 pathway #MMPMID28284058 Rybarczyk P ; Vanlaeys A ; Brassart B ; Dhennin-Duthille I ; Chatelain D ; Sevestre H ; Ouadid-Ahidouch H ; Gautier M Neoplasia 2017[Apr]; 19 (4 ): 288-300 PMID28284058 show ga Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a very poor prognosis. There is an urgent need to better understand the molecular mechanisms that regulate PDAC cell aggressiveness. The transient receptor potential melastatin 7 (TRPM7) is a nonselective cationic channel that mainly conducts Ca(2+) and Mg(2+). TRPM7 is overexpressed in numerous malignancies including PDAC. In the present study, we used the PANC-1 and MIA PaCa-2 cell lines to specifically assess the role of TRPM7 in cell invasion and matrix metalloproteinase secretion. We show that TRPM7 regulates Mg(2+) homeostasis and constitutive cation entry in both PDAC cell lines. Moreover, cell invasion is strongly reduced by TRPM7 silencing without affecting the cell viability. Conditioned media were further studied, by gel zymography, to detect matrix metalloproteinase (MMP) secretion in PDAC cells. Our results show that MMP-2, urokinase plasminogen activator (uPA), and heat-shock protein 90? (Hsp90?) secretions are significantly decreased in TRPM7-deficient PDAC cells. Moreover, TRPM7 expression in human PDAC lymph node metastasis is correlated to the channel expression in primary tumor. Taken together, our results show that TRPM7 is involved in PDAC cell invasion through regulation of Hsp90?/uPA/MMP-2 proteolytic axis, confirming that this channel could be a promising biomarker and possibly a target for PDAC metastasis therapy. |*Signal Transduction [MESH] |Calcium/metabolism [MESH] |Cell Line, Tumor [MESH] |Gene Expression [MESH] |Gene Silencing [MESH] |HSP90 Heat-Shock Proteins/*metabolism [MESH] |Humans [MESH] |Lymphatic Metastasis [MESH] |Magnesium/metabolism [MESH] |Matrix Metalloproteinase 2/*metabolism [MESH] |Models, Biological [MESH] |Pancreatic Neoplasms/genetics/*metabolism/pathology [MESH] |Protein Binding [MESH] |Protein Serine-Threonine Kinases/genetics/*metabolism [MESH] |Proteolysis [MESH] |TRPM Cation Channels/genetics/*metabolism [MESH]The Transient Receptor Potential Melastatin 7 Channel Regulates Pancre(epmc).pdf DeepDyve Pubget Overpricing