Fig. 8From: Phosphorylation of NF-κBp65 drives inflammation-mediated hepatocellular carcinogenesis and is a novel therapeutic targetAkt/mTOR signalling, and the ARRB1 promoter were activated through ARRB1-mediated NF-κBp65 phosphorylation at Ser536. a NF-κBp65 overexpression increased the expression of p-Akt, p-GSK3β and p-m-TOR in HepG2 and HepG3B cell lines. b, c p65 Ser536A (inactive) overexpression slightly increased, while p65 Ser536E (active) overexpression resulted in arrested increases in the expression of p-Akt, p-GSK3β and p-m-TOR in HepG2 and HepG3B cell lines. d p65 Ser536E (active) overexpression significantly increased the expression of p-m-TOR in HepG2 and HepG3B cell lines. e p65 Ser536A (inactive) overexpression slightly increased, while p65 Ser536E (active) overexpression obviously increased the activity of ARRB1 promoter, but not the p65 promoter, in 293 T cells. All values are mean ± SD. P < 0.05 using Student’s t-testBack to article page