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10.1152/ajplung.00125.2014 http://scihub22266oqcxt.onion/10.1152/ajplung.00125.2014 C4166785!4166785 !25038189     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25038189 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Physiol+Lung+Cell+Mol+Physiol 2014 ; 307 (6 ): L497-508 Nephropedia Template TP {{tp|p=25038189 |t=2014. Promotion of lung tumor growth by interleukin-17 |pdf=|usr=}}{{25038189 }} gab.com Text Promotion of lung tumor growth by interleukin-17 JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25038189 #FOAvip Recent findings demonstrate that inhaled cigarette smoke, the predominant lung carcinogen, elicits a T helper 17 (Th17) inflammatory phenotype. Interleukin-17A (IL-17), the hallmark cytokine of Th17 inflammation, displays pro- and antitumorigenic properties in a manner that varies according to tumor type and assay system. To investigate the role of IL-17 in lung tumor growth, we used an autochthonous tumor model (K-Ras(LA1) mice) with lung delivery of a recombinant adenovirus that expresses IL-17A. Virus-mediated expression of IL-17A in K-Ras(LA1) mice at 8-10 wk of age doubled lung tumor growth in 3 wk relative to littermates that received a green fluorescent protein-expressing control adenovirus. IL-17 induced matrix metalloproteinase-9 (MMP-9) expression in vivo and in vitro. In accord with this finding, selective and specific inhibitors of MMP-9 repressed the increased motility and invasiveness of IL-17-treated lung tumor cells in culture. Knockdown or mutation of p53 promoted the motility of murine lung tumor cells and abrogated the promigratory role of IL-17. Coexpression of siRNA-resistant wild-type, but not mutant, human p53 rescued both IL-17-mediated migration and MMP-9 mRNA induction in p53 knockdown lung tumor cells. IL-17 increased MMP-9 mRNA stability by reducing interaction with the mRNA destabilizing serine/arginine-rich splicing factor 1 (SRSF1). Taken together, our results indicate that IL-17 stimulates lung tumor growth and regulates MMP-9 mRNA levels in a p53- and SRSF1-dependent manner. Twit Text FOAVip Promotion of lung tumor growth by interleukin-17 ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25038189 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25038189 #FOAvip English Wikipedia <ref>{{Cite pmid|25038189 }}</ref> Promotion of lung tumor growth by interleukin-17 #MMPMID25038189 Xu B ; Guenther JF ; Pociask DA ; Wang Y ; Kolls JK ; You Z ; Chandrasekar B ; Shan B ; Sullivan DE ; Morris GF Am J Physiol Lung Cell Mol Physiol 2014[Sep]; 307 (6 ): L497-508 PMID25038189 show ga Recent findings demonstrate that inhaled cigarette smoke, the predominant lung carcinogen, elicits a T helper 17 (Th17) inflammatory phenotype. Interleukin-17A (IL-17), the hallmark cytokine of Th17 inflammation, displays pro- and antitumorigenic properties in a manner that varies according to tumor type and assay system. To investigate the role of IL-17 in lung tumor growth, we used an autochthonous tumor model (K-Ras(LA1) mice) with lung delivery of a recombinant adenovirus that expresses IL-17A. Virus-mediated expression of IL-17A in K-Ras(LA1) mice at 8-10 wk of age doubled lung tumor growth in 3 wk relative to littermates that received a green fluorescent protein-expressing control adenovirus. IL-17 induced matrix metalloproteinase-9 (MMP-9) expression in vivo and in vitro. In accord with this finding, selective and specific inhibitors of MMP-9 repressed the increased motility and invasiveness of IL-17-treated lung tumor cells in culture. Knockdown or mutation of p53 promoted the motility of murine lung tumor cells and abrogated the promigratory role of IL-17. Coexpression of siRNA-resistant wild-type, but not mutant, human p53 rescued both IL-17-mediated migration and MMP-9 mRNA induction in p53 knockdown lung tumor cells. IL-17 increased MMP-9 mRNA stability by reducing interaction with the mRNA destabilizing serine/arginine-rich splicing factor 1 (SRSF1). Taken together, our results indicate that IL-17 stimulates lung tumor growth and regulates MMP-9 mRNA levels in a p53- and SRSF1-dependent manner. |*Cell Movement [MESH] |Animals [MESH] |Enzyme Stability/genetics [MESH] |Gene Knockdown Techniques [MESH] |Humans [MESH] |Interleukin-17/*biosynthesis/genetics [MESH] |Lung Neoplasms/genetics/*metabolism/pathology [MESH] |Matrix Metalloproteinase 9/biosynthesis/genetics [MESH] |Mice [MESH] |Mice, Transgenic [MESH] |Neoplasm Invasiveness [MESH] |Nuclear Proteins/biosynthesis/genetics [MESH] |Proto-Oncogene Proteins p21(ras)/genetics/metabolism [MESH] |RNA Splicing Factors [MESH] |RNA-Binding Proteins/biosynthesis/genetics [MESH] |Serine-Arginine Splicing Factors [MESH]Promotion of lung tumor growth by interleukin-17 (epmc).pdf DeepDyve Pubget Overpricing