This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Cai, H. Articles by Gescher, A. J. Search for Related Content PubMed PubMed Citation Articles by Cai, H. Articles by Gescher, A. J.

¹ Cancer Biomarkers and Prevention Group, Department of Cancer Studies and Molecular Medicine and ² Medical Research Council Toxicology Unit, University of Leicester, Leicester, United Kingdom

Requests for reprints: Andreas J. Gescher, Cancer Biomarkers and Prevention Group, Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester Royal Infirmary, Robert Kilpatrick Clinical Sciences Building, Leicester LE2 7LX, United Kingdom. Phone: 44-116-223-1856; Fax: 44-116-223-1855. E-mail: ag15{at}le.ac.uk

While brown rice is a staple dietary constituent in Asia, rice consumed in the Western world is generally white, obtained from brown rice by removal of the bran. Rice bran contains the flavone tricin, which has been shown to inhibit colon cancer cell growth. We tested the hypothesis that tricin interferes with adenoma formation in the Apc^Min mouse. Mice received tricin (0.2%) in their American Institute of Nutrition 93G diet throughout their postweaning life span (4–18 weeks). Consumption of tricin reduced numbers of intestinal adenomas by 33% (P < 0.05) compared with mice on control diet. We explored whether tricin may exert its effect via inhibition of cyclooxygenase (COX) enzymes. Its effect on COX activity was assessed in purified enzyme preparations in vitro and its ability to reduce prostaglandin E₂ (PGE₂) levels in human colon–derived human colon epithelial cell (HCEC) and HCA-7 cells in vitro and in Apc^Min mice in vivo. Tricin inhibited activity of purified COX-1 and COX-2 enzyme preparations with IC₅₀ values of 1 µmol/L. At 5 µmol/L, it reduced PGE₂ production in HCEC or HCA-7 cells by 36% (P < 0.01) and 35% (P < 0.05), respectively. COX-2 expression was reduced by tricin weakly in HCEC and unaffected in HCA-7 cells. PGE₂ levels in the small intestinal mucosa and blood of Apc^Min mice that had received tricin were reduced by 34% (P < 0.01) and 40% (P < 0.05), respectively, compared with control mice. The results suggest that tricin should be further evaluated as a putative colorectal cancer chemopreventive agent.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

³ R.D. Verschoyle, H. Cai, W.P. Steward, and A.J. Gescher, unpublished observation.

Received 5/20/05; revised 6/24/05; accepted 7/ 8/05.