EGCG, a major component of green tea, inhibits tumour growth by inhibitingVEGF induction in human colon carcinoma cells

Citation
Yd. Jung et al., EGCG, a major component of green tea, inhibits tumour growth by inhibitingVEGF induction in human colon carcinoma cells, BR J CANC, 84(6), 2001, pp. 844-850
Citations number
31
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
BRITISH JOURNAL OF CANCER
ISSN journal
00070920 → ACNP
Volume
84
Issue
6
Year of publication
2001
Pages
844 - 850
Database
ISI
SICI code
0007-0920(20010323)84:6<844:EAMCOG>2.0.ZU;2-V
Abstract
Catechins are key components of teas that have antiproliferative properties . We investigated the effects of green tea catechins on intracellular signa lling and VEGF induction in vitro in serum-deprived HT29 human colon cancer cells and in vivo on the growth of HT29 cells in nude mice. In the in vitr o studies, (-)-epigallocatechin gallate (EGCG), the most abundant catechin in green tea extract, inhibited Erk-1 and Erk-2 activation in a dose-depend ent manner. However, other tea catechins such as (-)-epigallocatechin (EGC) , (-)-epicatechin gallate (ECG), and (-)-epicatechin (EC) did not affect Er k-1 or 2 activation at a concentration of 30 muM. EGCG also inhibited the i ncrease of VEGF expression and promoter activity induced by serum starvatio n. In the in vivo studies, athymic BALB/c nude mice were inoculated subcuta neously with HT29 cells and treated with daily intraperitoneal injections o f EC (negative control) or EGCG at 1.5 mg day(-1) mouse(-1) starting 2 days after tumour cell inoculation. Treatment with EGCG inhibited tumour growth (58%), microvessel density (30%), and tumour cell proliferation (27%) and increased tumour cell apoptosis (1.9-fold) and endothelial cell apoptosis ( 3-fold) relative to the control condition (P< 0.05 for all comparisons). EG CG may exert at least part of its anticancer effect by inhibiting angiogene sis through blocking the induction of VEGF. (C) 2001 Cancer Research Campai gn http://www.bjcancer.com.