Cargando…

miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma

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 repl...

Descripción completa

Detalles Bibliográficos
Autores principales: Wu, Hong-Jie, Zhuo, Ya, Zhou, Yan-Cai, Wang, Xin-Wei, Wang, Yan-Ping, Si, Chang-Yun, Wang, Xin-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504372/
https://www.ncbi.nlm.nih.gov/pubmed/28740345
http://dx.doi.org/10.3748/wjg.v23.i25.4569
_version_ 1783249279589023744
author Wu, Hong-Jie
Zhuo, Ya
Zhou, Yan-Cai
Wang, Xin-Wei
Wang, Yan-Ping
Si, Chang-Yun
Wang, Xin-Hong
author_facet Wu, Hong-Jie
Zhuo, Ya
Zhou, Yan-Cai
Wang, Xin-Wei
Wang, Yan-Ping
Si, Chang-Yun
Wang, Xin-Hong
author_sort Wu, Hong-Jie
collection PubMed
description 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.
format Online
Article
Text
id pubmed-5504372
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher Baishideng Publishing Group Inc
record_format MEDLINE/PubMed
spelling pubmed-55043722017-07-24 miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma Wu, Hong-Jie Zhuo, Ya Zhou, Yan-Cai Wang, Xin-Wei Wang, Yan-Ping Si, Chang-Yun Wang, Xin-Hong World J Gastroenterol Basic Study 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. Baishideng Publishing Group Inc 2017-07-07 2017-07-07 /pmc/articles/PMC5504372/ /pubmed/28740345 http://dx.doi.org/10.3748/wjg.v23.i25.4569 Text en ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ 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.
spellingShingle Basic Study
Wu, Hong-Jie
Zhuo, Ya
Zhou, Yan-Cai
Wang, Xin-Wei
Wang, Yan-Ping
Si, Chang-Yun
Wang, Xin-Hong
miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma
title miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma
title_full miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma
title_fullStr miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma
title_full_unstemmed miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma
title_short miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma
title_sort mir-29a promotes hepatitis b virus replication and expression by targeting smarce1 in hepatoma carcinoma
topic Basic Study
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504372/
https://www.ncbi.nlm.nih.gov/pubmed/28740345
http://dx.doi.org/10.3748/wjg.v23.i25.4569
work_keys_str_mv AT wuhongjie mir29apromoteshepatitisbvirusreplicationandexpressionbytargetingsmarce1inhepatomacarcinoma
AT zhuoya mir29apromoteshepatitisbvirusreplicationandexpressionbytargetingsmarce1inhepatomacarcinoma
AT zhouyancai mir29apromoteshepatitisbvirusreplicationandexpressionbytargetingsmarce1inhepatomacarcinoma
AT wangxinwei mir29apromoteshepatitisbvirusreplicationandexpressionbytargetingsmarce1inhepatomacarcinoma
AT wangyanping mir29apromoteshepatitisbvirusreplicationandexpressionbytargetingsmarce1inhepatomacarcinoma
AT sichangyun mir29apromoteshepatitisbvirusreplicationandexpressionbytargetingsmarce1inhepatomacarcinoma
AT wangxinhong mir29apromoteshepatitisbvirusreplicationandexpressionbytargetingsmarce1inhepatomacarcinoma