Conclusions
MiRNA-520a inhibited AKT gene expression and suppressed HBV transcription and replication. These findings suggest that miRNA-520a may be a novel target for the treatment of HBV infection because miRNA-520a reduced HepG2.2.15 cell survival and inhibited HBV replication associated with the AKT signalling pathway.
Methods
The effects of miR-520a on the proliferation, mitotic index and apoptosis of the HBV-replicating human hepatocellular carcinoma cell line HepG2.2.15 were measured using standard laboratory methods including flow cytometry. The effects of miR-520a on HBV transcription and replication were assessed using methods including immunoassays and reverse transcription-polymerase chain reaction. The effect of small interfering RNA (siRNA) to AKT on the levels of AKT mRNA and protein were also evaluated.
Objective
To investigate whether the mechanism by which a microRNA, miR-520a, suppresses the replication of hepatitis B virus (HBV) involves the regulation of the serine/threonine kinase ( AKT) gene.
Results
In HepG2.2.15 cells, miRNA-520a reduced HBV transcription and replication by reducing AKT levels. MiRNA-520a decreased cell proliferation and mitosis entry of cells and increased apoptosis in HepG2.2.15 cells. AKT levels were reduced significantly by its siRNA, which resulted in suppression of HBV replication in HepG2.2.15 cells. Conclusions: MiRNA-520a inhibited AKT gene expression and suppressed HBV transcription and replication. These findings suggest that miRNA-520a may be a novel target for the treatment of HBV infection because miRNA-520a reduced HepG2.2.15 cell survival and inhibited HBV replication associated with the AKT signalling pathway.