MSI2 knockdown represses extrahepatic cholangiocarcinoma growth and invasion by inhibiting epithelial–mesenchymal transition
Authors Hu F, Liu C, Xie F, Lin X, Yang J, Wang C, Huang Q
Received 11 April 2018
Accepted for publication 5 June 2018
Published 13 July 2018 Volume 2018:11 Pages 4035—4046
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr XuYu Yang
Feihu Hu,1,2 Chenhai Liu,1,2 Fang Xie,1,2 Xiansheng Lin,1,2 Ji Yang,1,2 Chao Wang,1,2 Qiang Huang1,2
1Department of General Surgery, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei, China; 2Anhui Province Key Laboratory of Hepatopancreatobiliary Surgery, Anhui Provincial Hospital, Heifei, China
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.
Keywords: Musashi2, cholangiocarcinoma, prognosis, metastasis, EMT
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