HBx-induced reactive oxygen species activates hepatocellular carcinogenesis via dysregulation of PTEN/Akt pathway

Figure 4 Effect of reactive oxygen species on phosphatase and tensin homolog oxidation, Akt pathway and hepatitis B virus X-protein expression. A, B: H₂O₂ treatment induced phosphatase and tensin homolog (PTEN) oxidation and activation of Akt pathway (increased relative p-Akt/total Akt ratio, cyclin D1 expression). Reactive oxygen species (ROS) scavenging through N-acetylcysteine (NAC) treatment reduced PTEN oxidation and Akt pathway; C: ROS effect on hepatitis B virus X-protein (HBx) expression, by quantitative reverse transcriptase polymerase chain reaction; D: Proposed scheme for ROS effect for activating Akt pathway via PTEN oxidation in HBx-induced hepatocarcinogenesis.