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10.3892/or.2016.5146 http://scihub22266oqcxt.onion/10.3892/or.2016.5146 C5112615!5112615!27748883     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27748883&cmd=llinks): Failed to open stream: HTTP request failed! 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Effect of RhoC on the epithelial-mesenchymal transition process induced by TGF-?1 in lung adenocarcinoma cells |pdf=|usr=}}{{27748883}} gab.com Text Effect of RhoC on the epithelial-mesenchymal transition process induced by TGF- 1 in lung adenocarcinoma cells JO: Oncol Rep http://www.kidney.de/pget.php?&tw=1&pmid=27748883 #FOAvip According to recent research, Ras homolog gene family member C (RhoC) is confirmed to have a powerful regulatory effect on cell motility mediated by the cytoskeleton, and this process is closely associated with tumor invasion and metastasis. In addition, the epithelial-mesenchymal transition (EMT) process which causes cytoskeleton rearrangement, also plays a pivotal role in tumor invasion and metastasis. Consequently, in the present study, we aimed to ascertain whether RhoC has an effect on the EMT process induced by TGF-?1 in lung adenocarcinoma cells and whether RhoC promotes tumor invasion by mediating the occurrence of EMT. Based on the findings, we demonstrated that RhoC was an essential mediator of the EMT process in lung adenocarcinoma cell line A549 which was evaluated by observing the morphological characteristics of the cells and by assessing the expression levels of two EMT marker proteins: E-cadherin and vimentin. During the process of EMT in the A549 cells induced by TGF-?1 (5 ng/ml), upregulated RhoC protein and RhoC activity were detected, which was associated with the enhanced invasive capability of the cells in vitro. Conversely, downregulation of the expression of RhoC by shRNA markedly impeded EMT progression as well as the invasion of A549 cells. Our results may provide a novel target towards the prevention of metastasis in advanced lung adenocarcinoma. Twit Text FOAVip Effect of RhoC on the epithelial-mesenchymal transition process induced by TGF- 1 in lung adenocarcinoma cells ????Oncol Rep http://www.kidney.de/pget.php?&tw=1&pmid=27748883 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27748883 #FOAvip English Wikipedia <ref>{{Cite pmid|27748883}}</ref> Effect of RhoC on the epithelial-mesenchymal transition process induced by TGF-?1 in lung adenocarcinoma cells #MMPMID27748883 Lu X; Guo H; Chen X; Xiao J; Zou Y; Wang W; Chen Q Oncol Rep 2016[Dec]; 36 (6): 3105-12 PMID27748883show ga According to recent research, Ras homolog gene family member C (RhoC) is confirmed to have a powerful regulatory effect on cell motility mediated by the cytoskeleton, and this process is closely associated with tumor invasion and metastasis. In addition, the epithelial-mesenchymal transition (EMT) process which causes cytoskeleton rearrangement, also plays a pivotal role in tumor invasion and metastasis. Consequently, in the present study, we aimed to ascertain whether RhoC has an effect on the EMT process induced by TGF-?1 in lung adenocarcinoma cells and whether RhoC promotes tumor invasion by mediating the occurrence of EMT. Based on the findings, we demonstrated that RhoC was an essential mediator of the EMT process in lung adenocarcinoma cell line A549 which was evaluated by observing the morphological characteristics of the cells and by assessing the expression levels of two EMT marker proteins: E-cadherin and vimentin. During the process of EMT in the A549 cells induced by TGF-?1 (5 ng/ml), upregulated RhoC protein and RhoC activity were detected, which was associated with the enhanced invasive capability of the cells in vitro. Conversely, downregulation of the expression of RhoC by shRNA markedly impeded EMT progression as well as the invasion of A549 cells. Our results may provide a novel target towards the prevention of metastasis in advanced lung adenocarcinoma. äEffect of RhoC on the epithelial-mesenchymal transition process induce(epmc).pdf DeepDyve Pubget Overpricing