Home CONTACT Neoplasma Ahead of print Neoplasma Vol.67, No.4, p.735–742, 2020

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Neoplasma Vol.67, No.4, p.735–742, 2020

Title: Regulation of HBV replication and gene expression by miR-501-3p via targeting ZEB2 in hepatocellular carcinoma
Author: Z. J. Zhong, J. F. Xu, Z. Z. Li, W. Y. Zhou, X. X. Chen, J. H. Zhou, Z. Y. Li

Abstract: Hepatitis B virus (HBV) infection is a major public health issue with serious medical consequences. The roles of microRNAs (miRNAs) in HBV replication and expression have been generally recognized, and the abnormal expression of miR-501 has been reported in patients with HBV infection. However, the function and mechanism in HBV replication remain elusive. The expression patterns of miR-501-3p and ZEB2 in HBV-related hepatocellular carcinoma (HCC) tissues and HBV-expressing HCC cells were determined by qRT-PCR and western blot assays. HBV replication and expression were evaluated through detecting the copies of HBV DNA and the secretion of HBV surface antigens HBsAg and HBeAg by real-time PCR and ELISA analyses. Bioinformatics and dual-luciferase reporter analyses were employed to validate the functional interaction between miR-501-3p and ZEB2. miR-501-3p was significantly upregulated, while ZEB2 was downregulated in HBV-related HCC tissues and cells compared with relative controls without HBV infection. Knockdown of miR-501-3p hampered HBV replication and gene expression in HepG2.2.15 and HepAD38 cells. ZEB2 was identified as a functional target of miR-501-3p. The absence of ZEB2 abolished the inhibitory effects of anti-miR-501-3p on HBV replication and gene expression. Our data indicated that miR-501-3p participated in the regulation of HBV replication and gene expression partially via repressing ZEB2 in HepG2.2.15 and HepAD38 cells, providing a promising antiviral avenue for HBV infection.

Keywords: Hepatitis B virus, miR-501-3p, ZEB2, replication, expression, hepatocellular carcinoma
Published online: 08-May-2020
Year: 2020, Volume: 67, Issue: 4 Page From: 735, Page To: 742

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