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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2018
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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. |
format | Online Article Text |
id | pubmed-6049051 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
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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