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10.2147/OTT.S170739 http://scihub22266oqcxt.onion/10.2147/OTT.S170739 C6049051!6049051!30034243     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30034243&cmd=llinks): Failed to open stream: HTTP request failed! 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MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial?mesenchymal transition |pdf=|usr=}}{{30034243}} gab.com Text MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial mesenchymal transition JO: Onco Targets Ther http://www.kidney.de/pget.php?&tw=1&pmid=30034243 #FOAvip Purpose: To investigate the expression and functional role of Musashi2 (MSI2), an RNA-binding protein, in extrahepatic cholangiocarcinoma (eCCA). Patients and methods: We measured MSI2 expression in human specimens and cell lines using Western blot and quantitative real-time polymerase chain reaction, and we analyzed its association with clinicopathologic features in eCCA patients. Univariate and multivariate analyses were performed to identify risk factors correlated with overall survival and disease-free survival. Functional experiments were used to study the mechanisms of MSI2 in regulating eCCA cell growth, migration, and invasion. Results: MSI2 expression was upregulated significantly in both human specimens and cell lines, and high MSI2 expression was associated with lymph node metastasis, advanced TNM stage, and poor prognosis in eCCA patients. Additionally, MSI2 overexpression promoted eCCA cell growth, migration, and invasion, while MSI2 knockdown repressed eCCA cell migration and invasion by inhibiting epithelial?mesenchymal transition. Conclusion: MSI2 is an independent prognostic factor for eCCA patients, and MSI2 downregulation inhibits eCCA cell growth and metastasis. MSI2 may be a potential therapeutic target for eCCA patients. Twit Text FOAVip MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial mesenchymal transition ????Onco Targets Ther http://www.kidney.de/pget.php?&tw=1&pmid=30034243 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30034243 #FOAvip English Wikipedia <ref>{{Cite pmid|30034243}}</ref> MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial?mesenchymal transition #MMPMID30034243 Hu F; Liu C; Xie F; Lin X; Yang J; Wang C; Huang Q Onco Targets Ther 2018[]; 11 (ä): 4035-46 PMID30034243show ga Purpose: To investigate the expression and functional role of Musashi2 (MSI2), an RNA-binding protein, in extrahepatic cholangiocarcinoma (eCCA). Patients and methods: We measured MSI2 expression in human specimens and cell lines using Western blot and quantitative real-time polymerase chain reaction, and we analyzed its association with clinicopathologic features in eCCA patients. Univariate and multivariate analyses were performed to identify risk factors correlated with overall survival and disease-free survival. Functional experiments were used to study the mechanisms of MSI2 in regulating eCCA cell growth, migration, and invasion. Results: MSI2 expression was upregulated significantly in both human specimens and cell lines, and high MSI2 expression was associated with lymph node metastasis, advanced TNM stage, and poor prognosis in eCCA patients. Additionally, MSI2 overexpression promoted eCCA cell growth, migration, and invasion, while MSI2 knockdown repressed eCCA cell migration and invasion by inhibiting epithelial?mesenchymal transition. Conclusion: MSI2 is an independent prognostic factor for eCCA patients, and MSI2 downregulation inhibits eCCA cell growth and metastasis. MSI2 may be a potential therapeutic target for eCCA patients. äMSI2 knockdown represses extrahepatic cholangiocarcinoma growth and in(epmc).pdf DeepDyve Pubget Overpricing