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Carcinogenesis Advance Access originally published online on February 12, 2006
Carcinogenesis 2006 27(7):1465-1474; doi:10.1093/carcin/bgi349
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Resveratrol inhibits phorbol ester-induced expression of COX-2 and activation of NF-{kappa}B in mouse skin by blocking I{kappa}B kinase activity

Joydeb Kumar Kundu, Young Kee Shin, Sung Hoon Kim 1 and Young-Joon Surh *

National Research Laboratory of Molecular Carcinogenesis and Chemoprevention, College of Pharmacy, Seoul National University, Seoul 151-742 and 1 Graduate School of East-West Medical Science, Kyunghee University, Yongin 449-701, Korea

* To whom correspondence should be addressed at: College of Pharmacy, Seoul National University, Shillim-dong, Kwanak-ku, Seoul 151-742, Korea. Tel: +82 2 880 7845; Fax: +82 2 874 9775; Email: surh{at}plaza.snu.ac.kr

Aberrant expression of cyclooxygenase-2 (COX-2) has been implicated in tumor promotion. Resveratrol, a phytoalexin present in grapes, was reported to inhibit multistage mouse skin carcinogenesis. In the present study, we found that topically applied resveratrol significantly inhibited COX-2 expression induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Resveratrol-suppressed phosphorylation and subsequent degradation of I{kappa}B{alpha}, thereby inhibiting activation of nuclear factor-{kappa}B (NF-{kappa}B) in TPA-stimulated mouse skin. Pretreatment with resveratrol also suppressed TPA-induced phosphorylation of extracellular signal-regulated protein kinase (ERK) and p38 mitogen-activated protein (MAP) kinase. Resveratrol blunted TPA-induced phosphorylation of p65 and its interaction with CBP/p300, rendering NF-{kappa}B transcriptionally inactive. To get further insights into the molecular basis of NF-{kappa}B inactivation by resveratrol, we examined the role of I{kappa}B kinase (IKK) in mediating TPA-induced activation of NF-{kappa}B and COX-2 expression. TPA treatment led to rapid induction of IKK activity in mouse skin, which was abolished either by resveratrol or an IKK inhibitor Bay 11-7082. Topical application of Bay 11-7082 also abrogated TPA-induced NF-{kappa}B activation and COX-2 expression, supporting the involvement of IKK in TPA-induced COX-2 expression. Taken together, the above findings suggest that resveratrol targets IKK in blocking TPA-induced NF-{kappa}B activation and COX-2 expression in mouse skin in vivo.


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