MicroRNA-137 promotes hepatitis B virus gene expression and replication via targeting the protein inhibitor of activated STAT 2.

Hepatitis B virus (HBV) infection is one of the most important infectious diseases in China. In this study, we investigated the functional role of miR-137 in HBV infection to further elucidate the mechanism underlying the associated pathology. Viral replication was determined after transfection of HEK293 cells with the replication-competent vector pHBV1.3 and miR137 mimics or inhibitors. Expression of HBV genes was determined by quantitative real-time PCR (qRT-PCR). Expression of miR-137 and protein inhibitor of activated STAT 2 (PIAS2) was determined by qRT-PCR and Western blotting. Activity of the PIAS2 3'-UTR was determined by dual-luciferase reporter assays. Transfection of HEK293 cells with pHBV1.3 increased the expression of miR-137. Co-transfection with miR-137 mimic upregulated HBV gene expression and viral replication. MiR-137 targeted the PIAS2 3'-UTR, and suppressed PIAS2 mRNA and protein expressions. SiRNA-mediated PIAS2 knockdown suppressed HBV gene expression and viral replication. PIAS2 expression rescued the promotion effect of miR-137 on HBV expression and viral replication. MiR-137 expression was significantly upregulated following HBV infection. Furthermore, miR-137 promoted the expression of HBV genes and viral replication by targeting the expression of PIAS2. Our findings might provide a new insight into the diagnosis and treatment of HBV infection.