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10.18632/oncotarget.16404 http://scihub22266oqcxt.onion/10.18632/oncotarget.16404 C5503575!5503575!28418915     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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2017 ; 8 (24): 38825-40 Nephropedia Template TP {{tp|p=28418915|t=2017. MTA1 promotes epithelial to mesenchymal transition and metastasis in non-small-cell lung cancer |pdf=|usr=}}{{28418915}} gab.com Text MTA1 promotes epithelial to mesenchymal transition and metastasis in non-small-cell lung cancer JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28418915 #FOAvip The present study assessed the role of metastasis-associated protein 1 (MTA1) in epithelial to mesenchymal transition (EMT) and metastasis in non-small-cell lung cancer (NSCLC) cells using a normal lung epithelium cell line, three NSCLC cell lines, a mouse NSCLC model, and 56 clinical NSCLC samples. We observed that MTA1 overexpression decreased cellular adhesion, promoted migration and invasion, and changed cytoskeletal polarity. MTA1 knockdown had the opposite effects. MTA1 overexpression decreased E-cadherin, Claudin-1, and ZO-1 levels and increased Vimentin expression in vitro and in vivo, through activation of AKT/GSK3?/?-catenin signaling. However, treatment with the AKT inhibitor MK2206 did not completely rescue effects associated with MTA1 expression changes, indicating that pathways other than the AKT/GSK3?/?-catenin pathway could be involved in MTA1-induced EMT. Compared with normal lung tissues, MTA1 expression was elevated in NSCLC patient tissues and was correlated with American Joint Committee on Cancer stage, T stage, lymphatic metastasis, and patient overall survival. Additionally, MTA1 expression was positively associated with p-AKT and cytoplasmic ?-catenin levels. These findings indicate MTA1 promotes NSCLC cell EMT and metastasis via AKT/GSK3?/?-catenin signaling, which suggests MTA1 may be an effective anti-NSCLC therapeutic target. Twit Text FOAVip MTA1 promotes epithelial to mesenchymal transition and metastasis in non-small-cell lung cancer ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28418915 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28418915 #FOAvip English Wikipedia <ref>{{Cite pmid|28418915}}</ref> MTA1 promotes epithelial to mesenchymal transition and metastasis in non-small-cell lung cancer #MMPMID28418915 Ma K; Fan Y; Dong X; Dong D; Guo Y; Wei X; Ning J; Geng Q; Wang C; Hu Y; Li M; Niu W; Li E; Wu Y Oncotarget 2017[Jun]; 8 (24): 38825-40 PMID28418915show ga The present study assessed the role of metastasis-associated protein 1 (MTA1) in epithelial to mesenchymal transition (EMT) and metastasis in non-small-cell lung cancer (NSCLC) cells using a normal lung epithelium cell line, three NSCLC cell lines, a mouse NSCLC model, and 56 clinical NSCLC samples. We observed that MTA1 overexpression decreased cellular adhesion, promoted migration and invasion, and changed cytoskeletal polarity. MTA1 knockdown had the opposite effects. MTA1 overexpression decreased E-cadherin, Claudin-1, and ZO-1 levels and increased Vimentin expression in vitro and in vivo, through activation of AKT/GSK3?/?-catenin signaling. However, treatment with the AKT inhibitor MK2206 did not completely rescue effects associated with MTA1 expression changes, indicating that pathways other than the AKT/GSK3?/?-catenin pathway could be involved in MTA1-induced EMT. Compared with normal lung tissues, MTA1 expression was elevated in NSCLC patient tissues and was correlated with American Joint Committee on Cancer stage, T stage, lymphatic metastasis, and patient overall survival. Additionally, MTA1 expression was positively associated with p-AKT and cytoplasmic ?-catenin levels. These findings indicate MTA1 promotes NSCLC cell EMT and metastasis via AKT/GSK3?/?-catenin signaling, which suggests MTA1 may be an effective anti-NSCLC therapeutic target. äMTA1 promotes epithelial to mesenchymal transition and metastasis in n(epmc).pdf DeepDyve Pubget Overpricing