Figure 3
From: The emerging role of hepatitis B virus Pre-S2 deletion mutant proteins in HBV tumorigenesis
Proposed model of HBV pre-S2 mutant-induced in metabolic disturbance and tumorigenesis. HBV pre-S2 mutant activated mTOR through ER stress-dependent VEGF-A/Akt signal cascade. The activated mTOR induced glycolysis via YY1/c-Myc/Glut1 signaing and promoted de novo lipogenesis through the activation of SREBP-1 and ACLY signals. The combined effects of aerobic glycolysis and de novo lipogenesis contributed to growth advantages of hepatocytes and subsequent HCC development.