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http://scihub22266oqcxt.onion/ C4859671!4859671!27186414     free     free     free       Am+J+Cancer+Res 2016 ; 6 (2): 440-51 Nephropedia Template TP {{tp|p=27186414|t=2016. IL-17 induces EMT via Stat3 in lung adenocarcinoma |pdf=|usr=}}{{27186414}} gab.com Text IL-17 induces EMT via Stat3 in lung adenocarcinoma JO: Am J Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27186414 #FOAvip Epithelial-mesenchymal transition (EMT) plays a vital role in lung inflammatory diseases, including lung cancer. However, the role and mechanism of action of the proinflammatory cytokine IL-17 in EMT in lung adenocarcinoma remain unresolved. In our study, we discovered that the expression of N-cadherin, Vimentin, Snail1, Snail2, and Twist1 was positively correlated with IL-17 expression, while E-cadherin expression was negatively correlated with IL-17 expression in human lung adenocarcinoma tissues. Moreover, we confirmed that IL-17 promoted EMT in A549 and Lewis lung carcinoma (LLC) cells in vitro by upregulating N-cadherin, Vimentin, Snail1, Snail2, and Twist1 expression and downregulating E-cadherin expression. Stat3 was activated in IL-17-treated A549 and LLC cells, and Stat3 inhibition or siRNA knockdown notably reduced IL-17-induced EMT in A549 and LLC cells. Thus, IL-17 promotes EMT in lung adenocarcinoma via Stat3 signaling; these observations suggest that targeting IL-17 and EMT are potential novel therapeutic strategies for lung cancer. Twit Text FOAVip IL-17 induces EMT via Stat3 in lung adenocarcinoma ????Am J Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27186414 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27186414 #FOAvip English Wikipedia <ref>{{Cite pmid|27186414}}</ref> IL-17 induces EMT via Stat3 in lung adenocarcinoma #MMPMID27186414 Huang Q; Han J; Fan J; Duan L; Guo M; Lv Z; Hu G; Chen L; Wu F; Tao X; Xu J; Jin Y Am J Cancer Res 2016[]; 6 (2): 440-51 PMID27186414show ga Epithelial-mesenchymal transition (EMT) plays a vital role in lung inflammatory diseases, including lung cancer. However, the role and mechanism of action of the proinflammatory cytokine IL-17 in EMT in lung adenocarcinoma remain unresolved. In our study, we discovered that the expression of N-cadherin, Vimentin, Snail1, Snail2, and Twist1 was positively correlated with IL-17 expression, while E-cadherin expression was negatively correlated with IL-17 expression in human lung adenocarcinoma tissues. Moreover, we confirmed that IL-17 promoted EMT in A549 and Lewis lung carcinoma (LLC) cells in vitro by upregulating N-cadherin, Vimentin, Snail1, Snail2, and Twist1 expression and downregulating E-cadherin expression. Stat3 was activated in IL-17-treated A549 and LLC cells, and Stat3 inhibition or siRNA knockdown notably reduced IL-17-induced EMT in A549 and LLC cells. Thus, IL-17 promotes EMT in lung adenocarcinoma via Stat3 signaling; these observations suggest that targeting IL-17 and EMT are potential novel therapeutic strategies for lung cancer. äIL-17 induces EMT via Stat3 in lung adenocarcinoma (epmc).pdf DeepDyve Pubget Overpricing