The role of NF-κB in PPARα-mediated hepatocarcinogenesis

Howard P. Glauert, Karen Calfee-Mason, Yixin Li, Vani Nilakantan, Michelle L. Twaroski, Job Tharappel, Brett T. Spear

Research output: Contribution to journalReview articlepeer-review

9 Scopus citations


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.

Original languageEnglish
Article number286249
JournalPPAR Research
StatePublished - 2008

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology (medical)


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