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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: Phosphorylation of NF-κBp65 drives inflammation-mediated hepatocellular carcinogenesis and is a novel therapeutic target

Fig. 7

Phosphorylation of NF-κBp65 induced Akt/mTOR signalling in an ARRB1-dependent manner. a, b L-p65 KO mice and ARRB1-KO mice were treated with either physiological saline (vehicle) or 100 mg/kg DEN intraperitoneal injection for 10 days. The protein levels of ARRB1, p-p65, p-Akt p-GSK-3 and m-TOR. Relative p-p65 level was scored (n = 6 in each group). All values are mean ± SD. P < 0.05 using Student’s t-test. (n = 6 in each group). c Representative images of p-p65 (top), p-GSK3β (middle) and PCNA (bottom) staining in DEN-induced L-p65 KO mouse liver inflammation. d ARRB1-overexpressing cells were established as described. The cellular lysates of ARRB1-transfected HepG2 cells were subjected to immunoprecipitation with an anti-GFP antibody. Coimmunoprecipitated endogenous p65 and p-p65 were detected. e TNF-α (40 ng/ml)-treated HepG2 cell lysates were subjected to immunoprecipitation with an anti-ARRB1 antibody. Coimmunoprecipitated endogenous p65 and p-p65 were detected with anti-p65 or p-p65 antibodies. Shown is a representative result of three experiments. IP = immunoprecipitated; IB = immunoblot

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