Role of NF-κB in Hepatocarcinogenesis and Its Potential Inhibition by Dietary Antioxidants

Howard      Perry Glauert

doi:10.2174/15680096112091160

Abstract

In this review, the role of nuclear factor-κB (NF-κB) in hepatocarcinogenesis is examined. The administration of several hepatic tumor promoters leads to the activation of NF-κB in the liver of rats and mice. Many studies support the hypothesis that the activation of NF-κB in the liver is inhibited by antioxidants. The role of NF-κB in hepatocarcinogenesis has been examined using NF-κB overexpression and knockout models. The role of NF-κB in liver carcinogenesis is complex; some models show that NF-κB contributes to carcinogenesis whereas others see no effect or an inhibition. Overall, although hepatic tumor promoting agents can activate NF-κB and this activation can be inhibited by antioxidants, the significance of this activation is unclear.

Keywords: Antioxidants, carcinogenesis, hepatocellular carcinomas, IκB kinase, NF-κB, vitamin E, peroxisome proliferator-activated receptor, TANK-binding kinase 1, tumor necrosis factor-α, constitutive androstane receptor, carbon tetrachloride, ciprofibrate, dimethylaminoazobenzene, diethylnitrosamine, glutathione peroxidase, reduced glutathione