In this study we examined the effects of antisense inhibition of miR-122 and transfection of a miR-122 mimic on HBV expression in hepatoma cells. The over-expression of miR-122 inhibited HBV expression, whereas the depletion of endogenous miR-122 resulted in increased production of HBV in transfected cells. We further found that the down-regulation of Heme oxygenase-1 (HO-1) by miR-122 plays a negative role in the miR-122-mediated inhibition of viral expression. Our study demonstrates the anti-HBV activity of miR-122, suggesting that therapies that increase miR-122 and HO-1 may be an effective strategy to limit HBV replication.
We listed the cellular functions of these relevant miRNAs in liver disease and their biological properties associated with HBV or HBV-related HCC in Table 1. We also summarized the known changes of miRNAs involved in multiple steps of chronic hepatitis B, from hepatitis to cirrhosis and finally to HCC (Fig. 3).