Objective      To explore the potential mechanism of hepatitis B virus X protein (HBX)-modulated miR-199a expression in hepatitis B virus (HBV) related hepatocarcinogenesis.       Methods      HepG2 cells were transfected with HBX-containing recombinant adenovirus (Ad-HBX)

and HepG2.2.15 cells capable of stably expressing HBV gene were transfected with siRNA-HBX. Fluorescence quantitative PCR was used for detecting mRNA expression levels of HBX

miR-199a

and AKT in HBV-related hepatocellular carcinoma tissues and hepatocellular carcinoma cells

while Western blotting was adopted to detect the protein expression of HBX and AKT. After transfection with miR-199a mimics and miR-199a inhibitor

quantitative PCR and Western blotting were employed to detect the expression of AKT in hepatocellular carcinoma cells.       Results      Experimental results showed that miR-199a expression in HepG2.2.15 cells was significantly lower than that in HepG2 cells

and down-regulation of miR-199a expression was related with HBX (P0.05). AKT expression in HepG2.2.15 cells was significantly higher than that in HepG2 cells (P0.05)

and over-expression of miR-199a in HepG2. 2.15 cells could significantly reduce AKT expression (P0.05)

while inhibition of miR-199a in HepG2 cells could significantly increase AKT expression (P0.05). In addition

the expression level of miR-199a in HBV-related hepatocellular carcinoma tissues was lower than that in the adjacent noncancer tissues.       Conclusion      HBX regulates the AKT expression through miR-199a

which may lead to HBV-related hepatocarcinogenesis.