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10.1371/journal.pone.0059410 http://scihub22266oqcxt.onion/10.1371/journal.pone.0059410 23555666!3610652!23555666     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2013 ; 8 (3): e59410 Nephropedia Template TP {{tp|p=23555666|t=2013. The decrease of mineralcorticoid receptor drives angiogenic pathways in colorectal cancer |pdf=|usr=}}{{23555666}} gab.com Text The decrease of mineralcorticoid receptor drives angiogenic pathways in colorectal cancer JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=23555666 #FOAvip Angiogenesis plays a crucial role in tumor growth and progression. Low expression of mineralocorticoid receptor (MR) in several malignant tumors correlates with disease recurrence and overall survival. Previous studies have shown that MR expression is decreased in colorectal cancer (CRC). Here we hypothesize that decreased MR expression can contribute to angiogenesis and poor patient survival in colorectal malignancies. In a cohort of CRC patients, we analyzed tumor MR expression, its correlation with tumor microvascular density and its impact on survival. Subsequently, we interrogated the role of MR in angiogenesis in an in vitro model, based on the colon cancer cell line HCT116, ingenierized to re-express a physiologically controlled MR. In CRC, decreased MR expression was associated with increased microvascular density and poor patient survival. In pchMR transfected HCT116, aldosterone or natural serum steroids largely inhibited mRNA expression levels of both VEGFA and its receptor 2/KDR. In CRC, MR activation may significantly decrease angiogenesis by directly inhibiting dysregulated VEGFA and hypoxia-induced VEGFA mRNA expression. In addition, MR activation attenuates the expression of the VEGF receptor 2/KDR, possibly dampening the activation of a VEGFA/KDR dependent signaling pathway important for the survival of tumor cells under hypoxic conditions. Twit Text FOAVip The decrease of mineralcorticoid receptor drives angiogenic pathways in colorectal cancer ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=23555666 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23555666 #FOAvip English Wikipedia <ref>{{Cite pmid|23555666}}</ref> The decrease of mineralcorticoid receptor drives angiogenic pathways in colorectal cancer #MMPMID23555666 Tiberio L; Nascimbeni R; Villanacci V; Casella C; Fra A; Vezzoli V; Furlan L; Meyer G; Parrinello G; Baroni MD; Salerni B; Schiaffonati L PLoS One 2013[]; 8 (3): e59410 PMID23555666show ga Angiogenesis plays a crucial role in tumor growth and progression. Low expression of mineralocorticoid receptor (MR) in several malignant tumors correlates with disease recurrence and overall survival. Previous studies have shown that MR expression is decreased in colorectal cancer (CRC). Here we hypothesize that decreased MR expression can contribute to angiogenesis and poor patient survival in colorectal malignancies. In a cohort of CRC patients, we analyzed tumor MR expression, its correlation with tumor microvascular density and its impact on survival. Subsequently, we interrogated the role of MR in angiogenesis in an in vitro model, based on the colon cancer cell line HCT116, ingenierized to re-express a physiologically controlled MR. In CRC, decreased MR expression was associated with increased microvascular density and poor patient survival. In pchMR transfected HCT116, aldosterone or natural serum steroids largely inhibited mRNA expression levels of both VEGFA and its receptor 2/KDR. In CRC, MR activation may significantly decrease angiogenesis by directly inhibiting dysregulated VEGFA and hypoxia-induced VEGFA mRNA expression. In addition, MR activation attenuates the expression of the VEGF receptor 2/KDR, possibly dampening the activation of a VEGFA/KDR dependent signaling pathway important for the survival of tumor cells under hypoxic conditions. |*Gene Expression Regulation, Neoplastic[MESH] |Adenocarcinoma/*blood supply/*genetics/mortality/pathology[MESH] |Aldosterone/pharmacology[MESH] |Biomarkers, Tumor/*genetics/metabolism[MESH] |Cell Hypoxia/drug effects/genetics[MESH] |Colorectal Neoplasms/*blood supply/*genetics/mortality/pathology[MESH] |Disease Progression[MESH] |HCT116 Cells[MESH] |Humans[MESH] |Neovascularization, Pathologic[MESH] |Prognosis[MESH] |Receptors, Mineralocorticoid/*genetics/metabolism[MESH] |Signal Transduction/drug effects[MESH] |Survival Analysis[MESH] |Transfection[MESH] |Vascular Endothelial Growth Factor A/*genetics/metabolism[MESH]The decrease of mineralcorticoid receptor drives angiogenic pathways i(epmc).pdf DeepDyve Pubget Overpricing