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J Cell Biochem. 2018 Dec;119(12):9720-9729. doi: 10.1002/jcb.27286. Epub 2018 Aug 26.

miR-383 promotes cholangiocarcinoma cell proliferation, migration, and invasion through targeting IRF1.

Wan P1,2, Chi X3, Du Q1, Luo J1,4, Cui X1,5, Dong K1,6, Bing Y1,7, Heres C1, Geller DA1.

Author information

1
Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania.
2
Department of Infectious Diseases, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
3
Department of Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, P.R. China.
4
Department of Surgery, The Second Affiliated Hospital of Xiangya Medical University, Changsha, China.
5
Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
6
Department of General Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
7
Department of Surgery, The First Affiliated Hospital of Zhengzhou Medical University, Zhengzhou, China.

Abstract

Interferon regulatory factor 1 (IRF1) has been found to serve as a tumor suppressor in cholangiocarcinoma, and enabled prediction of clinical progression and prognosis in our previous study. The objective of the current study is to screen and identify valuable microRNAs (miR), which target IRF1 to regulate cholangiocarcinoma cell proliferation, migration, and invasion. High expression of miR-383 was observed in cholangiocarcinoma tissues and cells. Meanwhile, we found the predicted binding site of miR-383 on the IRF1 3'-untranslated region (3'-UTR) according to the miR target database. The miR-383 expression was negatively related to IRF1 messeneger RNA (mRNA) and protein expression in cholangiocarcinoma tissue samples, and miR-383 negatively regulated IRF1 mRNA and protein expression in cholangiocarcinoma cells. Subsequently, we conducted a luciferase reporter assay to prove the predicted binding site miR-383 on IRF1 3'-UTR. Moreover, the results of the rescue study suggested that IRF1 was a functional target of miR-383 involved in regulating cholangiocarcinoma cell proliferation, migration, and invasion. Finally, we evaluated the clinical and prognostic significance of miR-383 in cholangiocarcinoma cases, and found that high expression of miR-383 was correlated with advanced tumor stage, large tumor size, present vascular invasion, and metastasis, and acted as an unfavorable independent prognostic factor. In conclusion, miR-383 serves as a tumor-suppressive miR to regulate cholangiocarcinoma cell proliferation, migration, and invasion via directly targeting IRF1.

KEYWORDS:

biomarker; cholangiocarcinoma; interferon regulatory factor 1; miR-383; microRNA

PMID:
30145803
DOI:
10.1002/jcb.27286

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