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MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition

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 reactio...

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Autores principales: Hu, Feihu, Liu, Chenhai, Xie, Fang, Lin, Xiansheng, Yang, Ji, Wang, Chao, Huang, Qiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6049051/
https://www.ncbi.nlm.nih.gov/pubmed/30034243
http://dx.doi.org/10.2147/OTT.S170739
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author Hu, Feihu
Liu, Chenhai
Xie, Fang
Lin, Xiansheng
Yang, Ji
Wang, Chao
Huang, Qiang
author_facet Hu, Feihu
Liu, Chenhai
Xie, Fang
Lin, Xiansheng
Yang, Ji
Wang, Chao
Huang, Qiang
author_sort Hu, Feihu
collection PubMed
description 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.
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spelling pubmed-60490512018-07-20 MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition Hu, Feihu Liu, Chenhai Xie, Fang Lin, Xiansheng Yang, Ji Wang, Chao Huang, Qiang Onco Targets Ther Original Research 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. Dove Medical Press 2018-07-13 /pmc/articles/PMC6049051/ /pubmed/30034243 http://dx.doi.org/10.2147/OTT.S170739 Text en © 2018 Hu et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Hu, Feihu
Liu, Chenhai
Xie, Fang
Lin, Xiansheng
Yang, Ji
Wang, Chao
Huang, Qiang
MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition
title MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition
title_full MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition
title_fullStr MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition
title_full_unstemmed MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition
title_short MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition
title_sort msi2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6049051/
https://www.ncbi.nlm.nih.gov/pubmed/30034243
http://dx.doi.org/10.2147/OTT.S170739
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