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Carcinogenesis Advance Access published online on July 17, 2007
Carcinogenesis, doi:10.1093/carcin/bgm161
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Green tea selectively targets initial stages of intestinal carcinogenesis in the AOM-ApcMin mouse model

Ala Y. Issa1, Suresh R. Volate1, Stephanie J. Muga2, Daniela Nitcheva3, Theresa Smith4 and Michael J. Wargovich2,*

1 Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29203
2 Department of Cell & Molecular Pharmacology, Medical University of South Carolina, Charleston, SC 29245
3 Department of Epidemiology and Biostatistics, School of Public Health
4 Department of Basic Pharmaceutical Sciences, College of Pharmacy, University of Columbia, SC 29208

* To whom correspondence should be addressed to: Michael J. Wargovich, Cancer Chemoprevention Program, Hollings Cancer Center, 86 Jonathan Lucas Street, PO Box 250955, Charleston, SC 29245, Tel. 843-792-7604; Fax. 843-792-3200; E-Mail: wargovic{at}musc.edu

One of the liabilities of the ApcMin mouse as a model for colon cancer is its lack of a robust tumor response in the large bowel. In our protocol, we treated the ApcMin mouse with azoxymethane (AOM), a colon selective carcinogen. This protocol induced a 4-fold increase in the number of colon tumors. We utilized this protocol to investigate the possible mechanisms of inhibition of colorectal carcinogenesis by green tea (GT). Mice received water or a 0.6 % (w/v) solution of GT as the only source of beverage. GT treatment commenced at the 8th week of age and lasted for either 4 or 8 weeks. GT significantly inhibited the formation of new adenomas, but was ineffective against larger tumors. Mechanistically, we investigated the effects of GT on the expression of biomarkers involved colon carcinogenesis. Western blotting analysis showed that GT decreased the total levels of the early carcinogenesis biomarker ß catenin (BC) and its downstream target cyclin D1 (CD1). In contrast, the expression of COX-2 was not altered. Immunohistochemical analysis showed that GT inhibited the formation of adenomas overexpressing BC and CD1, but did not reduce the number of COX-2 expressing adenomas. Our results suggest that green tea specifically targets initial stages of colon carcinogenesis; the time of administration of green tea is pivotal for effective chemoprevention. Beverage levels of GT are not likely to inhibit the progress of any large adenomas or adenocarcinomas existing prior to the tea administration.

Key Words: green tea • colon cancer • azoxymethane (AOM) • ApcMin mouse model • ß-catenin • COX-2 and cyclin D1

Received May 16, 2006; revised June 29, 2007; accepted June 29, 2007.


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