MicroRNA-1205 Suppresses Hepatocellular Carcinoma Cell Proliferation via a CSNK2B/CDK4 Axis

Author:

Li Xiang123,Xie Shujie123,Xia Qin123,Yan Jia123,Chen Shuhuai123,Shen Jia123ORCID

Affiliation:

1. Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, P.R. China

2. Ningbo Institute of Life and Health Industry, University of Chinese Academy of Sciences, Ningbo, P.R. China

3. Key Laboratory of Diagnosis and Treatment of Digestive System Tumors of Zhejiang Province, Ningbo, P.R. China

Abstract

Introduction: MicroRNAs (miRNAs) play important roles in the progression of hepatocellular carcinoma (HCC) via modulating expression of their targeting mRNAs. The present study aimed to investigate the role of miR-1205 in HCC cell proliferation and investigate the underlying molecular mechanism. Methods: The effects of miR-1205 on proliferation ability of HCC cell lines were explored in vitro and in vivo. Real-time quantitative PCR (qPCR) analysis was performed to determine miR-1205 expression in HCC tissues and cell lines. Online prediction tools and luciferase assays were used to identify potential target genes of miR-1205. Western blot analysis and dual-luciferase assays were conducted to screen key signaling pathway proteins regulated by miR-1205 and its’ target gene. Results: In vitro and in vivo experiments showed that miR-1205 inhibits the proliferation of HCC cells. Dual-luciferase assays showed that miR-1205 interacted with CSNK2B by directly targeting the miRNA-binding site in the CSNK2B sequence, and further qPCR analysis indicated that CSNK2B expression was increased in HCC tissues and negatively correlated with miR-1205 expression. Furthermore, CSNK2B significantly promoted HCC cell proliferation, and CSNK2B overexpression or knockdown attenuated the effects of miR-1205 overexpression or inhibition on HCC cell viability, respectively. Mechanistically, miR-1205 suppresses HCC cell proliferation via a CSNK2B/CDK4 axis. Conclusion: The present results indicated that miR-1205 suppressed HCC cell proliferation by directly targeting CSNK2B and thus inhibiting the CDK4/pRb cell cycle pathway.

Publisher

SAGE Publications

Subject

Cancer Research,Oncology

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