Carcinogenesis, Vol. 21, No. 10, 1885-1890,
October 2000
© 2000 Oxford University Press
Carcinogenesis |
Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced NF-
B activation by tea polyphenols, (–)-epigallocatechin gallate and theaflavins
The Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA
(–)-Epigallocatechin gallate (EGCG) and theaflavins are believed to be the key active components in tea for the chemoprevention of cancer. However, the molecular mechanisms by which EGCG and theaflavins block carcinogenesis are not clear. In the JB6 mouse epidermal cell line a tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), which causes cell transformation at high frequency, markedly induced NF-
B activation. We found that EGCG and theaflavins inhibited TPA-induced NF-B activity in a concentration-dependent manner. These polyphenols blocked TPA-induced phosphorylation of IB
at Ser32 in the same concentration range. Moreover, the NF-B sequence-specific DNA-binding activity induced by TPA was also inhibited by these polyphenols. These results suggest that inhibition of NF-B activation is also important in accounting for the anti-tumor promotion effects of EGCG and theaflavins.
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