MicroRNA-802 induces hepatitis B virus replication and replication through regulating SMARCE1 expression in hepatocellular carcinoma

• DOI: 10.1038/s41419-019-1999-x
• Publication Date: 2019-10-14T12:04:23Z
• Authors: Yuanyuan Wang; Jingmei Cao; Shiyun Zhang; Lei Sun; Yi Nan; Hong Yao; Jian Fan; Li Ying Zhu; Lei Yu
• Keywords: Gene Expression Regulation, Viral; 0301 basic medicine; Hepatitis B virus; Carcinoma, Hepatocellular; Chromosomal Proteins, Non-Histone; Liver Neoplasms; Apoptosis; Hep G2 Cells; Hepatitis B; Virus Replication; Article; 3. Good health; DNA-Binding Proteins; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; Humans; Cell Proliferation

AbstractGrowing evidences have indicated that microRNAs (miRNAs) can regulate hepatitis B virus (HBV) expression and replication, playing crucial roles in the development of HBV infection. Until now, the functional role and mechanism of miR-802 in HBV replication and expression remain unknown. We indicated that miR-802 expression was upregulated in the HBV-associated hepatocellular carcinoma (HCC) tissues compared with the adjacent noncancerous samples. In addition, we showed that the SMARCE1 expression level was downregulated in the HBV-associated HCC tissues compared with the adjacent noncancerous samples. miR-802 expression was negatively related with MARCE1 expression in HBV-associated HCC tissues. Moreover, miR-802 expression was upregulated, and SMARCE1 expression was downregulated in the HBV-infected HepG2.2.15 cells. Ectopic expression of miR-802 significantly enhanced HBV DNA replication, while knockdown of miR-802 significantly decreased HBV DNA replication. We showed that overexpression of miR-802 promoted HbsAg and HbeAg expression, while inhibition of miR-802 decreased HbsAg and HbeAg expression. Furthermore, we indicated that ectopic expression of SMARCE1 suppressed HBV DNA replication and decreased the expression level of HbsAg and HbeAg. Finally, we showed that overexpression of miR-802 promoted HBV DNA replication through regulating SMARCE1 expression. These results suggested the important roles of miR-802 on HBV expression and replication, which may shed new light on the development of treatment for HBV.