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

Figure 3 Effect of hepatitis B virus X-protein-induced endogenous reactive oxygen species and phosphatase and tensin homolog oxidation. Endogenous reactive oxygen species (ROS) level was examined by flow cytometry. A, B: Increased production of ROS in hepatitis B virus X-protein (HBx) primary hepatocytes compared to the wild-type hepatocytes and HepG2-HBx compared to the Mock cells. Oxidized phosphatase and tensin homolog (PTEN) was detected by N-ethylmaleimide alkylation, and non-reducing sodium dodecyl sulfate polyacrylamide gel electrophoresis; C: In the upper panel, 20 μg protein was loaded, and for the lower panel, 50 μg was loaded; D: Parallel experiments were performed with extracts from HepG2-Mock and HBx cell lines.