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Carcinogenesis, Vol. 20, No. 2, 237-242, February 1999
© 1999 Oxford University Press

Resveratrol suppresses cell transformation and induces apoptosis through a p53-dependent pathway

Chuanshu Huang, Wei-ya Ma, Angela Goranson and Zigang Dong1

The Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA

Resveratrol, a plant constituent enriched in the skin of grapes, is one of the most promising agents for the prevention of cancer. However, the mechanism of the anti-carcinogenic activity of resveratrol is not well understood. Here we offer a possible explanation of its anti-cancer effect. Resveratrol suppresses tumor promoter-induced cell transformation and markedly induces apoptosis, transactivation of p53 activity and expression of p53 protein in the same cell line and at the same dosage. Also, resveratrol-induced apoptosis occurs only in cells expressing wild-type p53 (p53+/+), but not in p53-deficient (p53–/–) cells, while there is no difference in apoptosis induction between normal lymphoblasts and sphingomyelinase-deficient cell lines. These results demonstrate for the first time that resveratrol induces apoptosis through activation of p53 activity, suggesting that its anti-tumor activity may occur through the induction of apoptosis.

Abbreviations: BME, basal medium Eagle; DMEM, Dulbecco's modified Eagle's medium; DMSO, dimethyl sulfoxide; EBV, Epstein–Barr virus; EGF, epidermal growth factor; FBS, fetal bovine serum; MEM, Eagle's minimal essential medium; SMase, sphingomyelinase; TPA, 12-O-tetradecanoylphorbol-13-acetate.

1 To whom correspondence should be addressed Email: zgdong{at}smig.net


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