Review
Cancer chemoprevention with green tea catechins by targeting receptor tyrosine kinases
Article first published online: 2 MAY 2011
DOI: 10.1002/mnfr.201000622
Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Issue

Molecular Nutrition & Food Research
Special Issue: Green Tea and Cancer
Volume 55, Issue 6, pages 832–843, June 2011
Additional Information
How to Cite
Shimizu, M., Adachi, S., Masuda, M., Kozawa, O. and Moriwaki, H. (2011), Cancer chemoprevention with green tea catechins by targeting receptor tyrosine kinases. Mol. Nutr. Food Res., 55: 832–843. doi: 10.1002/mnfr.201000622
Publication History
- Issue published online: 3 JUN 2011
- Article first published online: 2 MAY 2011
- Manuscript Accepted: 24 MAR 2011
- Manuscript Revised: 17 MAR 2011
- Manuscript Received: 9 DEC 2010
Funded by
- Grants-in-Aid from the Ministry of Education, Science, Sports and Culture of Japan. Grant Numbers: 22790638, 21590838
- Grant-in-Aid for the 3rd Term Comprehensive 10-year Strategy for Cancer Control from the Ministry of Health, Labor and Welfare of Japan
- Abstract
- Article
- References
- Cited By
Keywords:
- Colorectal cancer;
- EGCG;
- Hepatocellular carcinoma;
- Lipid rafts;
- Receptor tyrosine kinase
Abstract
Recent studies indicate that receptor tyrosine kinases (RTKs), which play important roles in cell proliferation, are one of the possible targets of green tea catechins (GTCs) in cancer cell growth inhibition. (−)-Epigallocatechin-3-gallate (EGCG), the major catechin in green tea, inhibits cell proliferation and induces apoptosis in various types of cancer cells, including colorectal cancer and hepatocellular carcinoma cells, by blocking the activation of the epidermal growth factor receptor (EGFR) family of RTKs. EGCG inhibits the activation of insulin-like growth factor-1 receptor (IGF-1R) and VEGFR2, the other members of the RTK family, and this effect is also associated with the anticancer and chemopreventive properties of this agent. EGCG suppresses the activation of EGFR in part by altering membrane lipid organization and causing the subsequent inhibition of the dimerization and activation of this receptor. Preliminary trials have shown that GTCs successfully prevent the development and progression of precancerous lesions, such as colorectal adenomas, without causing severe adverse effects. The present report reviews evidence indicating that GTCs exert anticancer and chemopreventive effects by inhibiting the activation of specific RTKs, especially EGFR, IGF-1R, and VEGFR2, and concludes that targeting RTKs and their related signaling pathways by using tea catechins could be a promising strategy for the prevention of human cancers.

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