Next Article in Journal
Density Functionals of Chemical Bonding
Next Article in Special Issue
Betulinic Acid for Cancer Treatment and Prevention
Previous Article in Journal
Ion-Molecule Reactions and Chemical Composition of Emanated from Herculane Spa Geothermal Sources
Previous Article in Special Issue
Synthesis and Biological Evaluation of a Novel Pentagastrin- Toxin Conjugate Designed for a Targeted Prodrug Monotherapy of Cancer
Int. J. Mol. Sci. 2008, 9(6), 1034-1049; doi:10.3390/ijms9061034
Review

Targeting Receptor Tyrosine Kinases for Chemoprevention by Green Tea Catechin, EGCG

* ,  and
Received: 12 May 2008; in revised form: 4 June 2008 / Accepted: 4 June 2008 / Published: 20 June 2008
(This article belongs to the Special Issue Natural Compounds for Cancer Treatment and Prevention)
View Full-Text   |   Download PDF [864 KB, uploaded 19 June 2014]   |   Browse Figures
Abstract: Tea is one of the most popular beverages consumed worldwide. Epidemiologic studies show an inverse relationship between consumption of tea, especially green tea, and development of cancers. Numerous in vivo and in vitro studies indicate strong chemopreventive effects for green tea and its constituents against cancers of various organs. (–)-Epigallocatechin-3-gallate (EGCG), the major catechin in green tea, appears to be the most biologically active constituent in tea with respect to inhibiting cell proliferation and inducing apoptosis in cancer cells. Recent studies indicate that the receptor tyrosine kinases (RTKs) are one of the critical targets of EGCG to inhibit cancer cell growth. EGCG inhibits the activation of EGFR (erbB1), HER2 (neu/erbB2) and also HER3 (neu/erbB3), which belong to subclass I of the RTK superfamily, in various types of human cancer cells. The activation of IGF-1 and VEGF receptors, the other members of RTK family, is also inhibited by EGCG. In addition, EGCG alters membrane lipid organization and thus inhibits the dimerization and activation of EGFR. Therefore, EGCG inhibits the Ras/MAPK and PI3K/Akt signaling pathways, which are RTK-related cell signaling pathways, as well as the activation of AP-1 and NF-κB, thereby modulating the expression of target genes which are associated with induction of apoptosis and cell cycle arrest in cancer cells. These findings are significant because abnormalities in the expression and function of RTKs and their downstream effectors play a critical role in the development of several types of human malignancies. In this paper we review evidence indicating that EGCG exerts anticancer effects, at least in part, through inhibition of activation of the specific RTKs and conclude that targeting RTKs and related signaling pathway by tea catechins might be a promising strategy for the prevention of human cancers.
Keywords: Tea catechins; EGCG; cell signaling pathway; RTK. Tea catechins; EGCG; cell signaling pathway; RTK.
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Export to BibTeX |
EndNote


MDPI and ACS Style

Shimizu, M.; Shirakami, Y.; Moriwaki, H. Targeting Receptor Tyrosine Kinases for Chemoprevention by Green Tea Catechin, EGCG. Int. J. Mol. Sci. 2008, 9, 1034-1049.

AMA Style

Shimizu M, Shirakami Y, Moriwaki H. Targeting Receptor Tyrosine Kinases for Chemoprevention by Green Tea Catechin, EGCG. International Journal of Molecular Sciences. 2008; 9(6):1034-1049.

Chicago/Turabian Style

Shimizu, Masahito; Shirakami, Yohei; Moriwaki, Hisataka. 2008. "Targeting Receptor Tyrosine Kinases for Chemoprevention by Green Tea Catechin, EGCG." Int. J. Mol. Sci. 9, no. 6: 1034-1049.


Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert