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Carcinogenesis Advance Access published online on April 16, 2004
Carcinogenesis, doi:10.1093/carcin/bgh163
© 2004 by Oxford University Press
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Received December 2, 2003
Revised March 11, 2004
Accepted April 3, 2004

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Curcumin impairs tumor suppressor p53 function in colon cancer cells

Philip J. Moos 1*, Kornelia Edes 1, James E. Mullally 2, Frank A. Fitzpatrick 3

1 Department of Oncological Sciences, University of Utah, Huntsman Cancer Institute, Salt Lake City, Utah, 84112
2 Department of Medicinal Chemistry, University of Utah, Huntsman Cancer Institute, Salt Lake City, Utah, 84112
3 Department of Oncological Sciences, University of Utah, Huntsman Cancer Institute, Salt Lake City, Utah, 84112; Department of Medicinal Chemistry, University of Utah, Huntsman Cancer Institute, Salt Lake City, Utah, 84112

* To whom correspondence should be addressed. E-mail: philip.moos{at}hci.utah.edu.


  Abstract

Curcumin (diferuloylmethane) is being considered as a potential chemopreventive agent in humans. In vitro it inhibits transcription by NF-{kappa}B, and the activity of lipoxygenase or cyclooxygenase enzymes, which facilitate tumor progression. In vivo it is protective in rodent models of chemical carcinogenesis. Curcumin contains an {alpha},{beta}-unsaturated ketone, a reactive chemical substituent that is responsible for its repression of NF-{kappa}B. In compounds other than curcumin this same electrophilic moiety is associated with inactivation of the tumor suppressor, p53. Here we report that curcumin behaves analogously to these compounds. It disrupts the conformation of p53 protein required for its serine phosphorylation; its binding to DNA; its transactivation of p53-responsive genes; and p53-mediated cell cycle arrest.

Key Words: Tumor suppressor p53, curcumin, molecular toxicology, iatrogenic effects, electrophile


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