The Role of NF-κB in PPARα-Mediated Hepatocarcinogenesis

In this review, the role of NF-κB in the induction of hepatocarcinogenesis by peroxisome proliferators is examined. The administration of peroxisome proliferators for more than a three-day period leads to the activation of NF-κB in the livers of rats and mice. On the other hand, peroxisome prolifera...

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Published in:PPAR Research 2008-01, Vol.2008 (2008), p.375-383-034
Main Authors: Calfee-Mason, Karen, Nilakantan, Vani, Glauert, Howard P., Spear, Brett T., Tharappel, Job, Twaroski, Michelle L., Li, Yixin
Format: Article
Language:English
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Review
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Summary:In this review, the role of NF-κB in the induction of hepatocarcinogenesis by peroxisome proliferators is examined. The administration of peroxisome proliferators for more than a three-day period leads to the activation of NF-κB in the livers of rats and mice. On the other hand, peroxisome proliferator activated receptor-α (PPARα) activation in non-hepatic tissues can lead to the inhibition of NF-κB activation. Several lines of evidence support the hypothesis that the activation of NF-κB by peroxisome proliferators in the liver is mediated by oxidative stress. The role of NF-κB in peroxisome proliferator-induced hepatocarcinogenesis has been examined using NF-κB knockout models. Specifically, the induction of cell proliferation and the promotion of liver carcinogenesis are inhibited in mice lacking the p50 subunit of NF-κB. Overall, the activation of NF-κB appears to be important in the carcinogenic activity of peroxisome proliferators.
ISSN:1687-4757
1687-4765
DOI:10.1155/2008/286249