Basic Study
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 7, 2017; 23(25): 4569-4578
Published online Jul 7, 2017. doi: 10.3748/wjg.v23.i25.4569
miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma
Hong-Jie Wu, Ya Zhuo, Yan-Cai Zhou, Xin-Wei Wang, Yan-Ping Wang, Chang-Yun Si, Xin-Hong Wang
Hong-Jie Wu, Ya Zhuo, Yan-Cai Zhou, Xin-Wei Wang, Yan-Ping Wang, Chang-Yun Si, Xin-Hong Wang, Department of Infectious Disease, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang 453100, Henan Province, China
Author contributions: This work was conceived and designed by Zhuo Y and Wang XH; the research was executed by Wu HJ, Zhou YC and Wang XW; data were analyzed by Wang YP and Si CY; the manuscript was written by Wu HJ and Zhuo Y.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board and Ethics Committee of Xinxiang Medical University.
Conflict-of-interest statement: The authors declare that there is no conflict of interest related to this study.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Xin-Hong Wang, Chief Physician, Department of Infectious Disease, The First Affiliated Hospital of Xinxiang Medical University, No. 88 Jiankang Road, Xinxiang 453100, Henan Province, China. wangxinh621@sina.com
Telephone: +86-373-4402712
Received: February 7, 2017
Peer-review started: February 9, 2017
First decision: March 16, 2017
Revised: March 27, 2017
Accepted: April 12, 2017
Article in press: April 12, 2017
Published online: July 7, 2017
Processing time: 149 Days and 18.6 Hours
Abstract
AIM

To investigate the functional role and underlying molecular mechanism of miR-29a in hepatitis B virus (HBV) expression and replication.

METHODS

The levels of miR-29a and SMARCE1 in HBV-infected HepG2.2.15 cells were measured by quantitative real-time PCR and western blot analysis. HBV DNA replication was measured by quantitative PCR and Southern blot analysis. The relative levels of hepatitis B surface antigen and hepatitis B e antigen were detected by enzyme-linked immunosorbent assay. The Cell Counting Kit-8 (CCK-8) was used to detect the viability of HepG2.2.15 cells. The relationship between miR-29a and SMARCE1 were identified by target prediction and luciferase reporter analysis.

RESULTS

miR-29a promoted HBV replication and expression, while SMARCE1 repressed HBV replication and expression. Cell viability detection indicated that miR-29a transfection had no adverse effect on the host cells. Moreover, SMARCE1 was identified and validated to be a functional target of miR-29a. Furthermore, restored expression of SMARCE1 could relieve the increased HBV replication and expression caused by miR-29a overexpression.

CONCLUSION

miR-29a promotes HBV replication and expression through regulating SMARCE1. As a potential regulator of HBV replication and expression, miR-29a could be a promising therapeutic target for patients with HBV infection.

Keywords: miR-29a; SMARCE1; Hepatitis B surface antigen; Hepatitis B virus replication; Hepatitis B e antigen

Core tip: Although aberrant miR-29a expression has been found to be involved in the process of hepatitis B virus (HBV) infection, its underlying mechanism remains unclear. In this study, we analyzed the expression levels of miR-29a in HBV-infected HepG2.2.15 cells. Our results indicated that miR-29a expression was up-regulated in HBV-associated hepatocellular carcinoma cells. In addition, SMARCE1 was confirmed to be a functional target of miR-29a. miR-29a promoted HBV replication and expression through directly regulating SMARCE1. These findings provide potential therapeutic targets for patients with HBV infection.