(-)-Epigallocatechin (EGC) of Green Tea Induces Apoptosis of Human Breast Cancer Cells But Not of their Normal Counterparts David Vergote Laboratoire de Biologie du Développement (UPRES-EA 1033), Equipe Polyphénols, Université des Sciences et Technologies de Lille, Villeneuve d’Ascq, France Cécile Cren-Olivé Laboratoire de Chimie Organique et Macromoléculaire (UPRESA-8009 CNRS), Equipe Polyphénols, Université des Sciences et Technologies de Lille, Villeneuve d’Ascq, France Valérie Chopin Laboratoire de Biologie du Développement (UPRES-EA 1033), Equipe Polyphénols, Université des Sciences et Technologies de Lille, Villeneuve d’Ascq, France Robert-Alain Toillon Laboratoire de Biologie du Développement (UPRES-EA 1033), Equipe Polyphénols, Université des Sciences et Technologies de Lille, Villeneuve d’Ascq, France Christian Rolando Laboratoire de Chimie Organique et Macromoléculaire (UPRESA-8009 CNRS), Equipe Polyphénols, Université des Sciences et Technologies de Lille, Villeneuve d’Ascq, France Hubert Hondermarck Laboratoire de Biologie du Développement (UPRES-EA 1033), Equipe Polyphénols, Université des Sciences et Technologies de Lille, Villeneuve d’Ascq, France Xuefen Le Bourhis Laboratoire de Biologie du Développement (UPRES-EA 1033), Equipe Polyphénols, Université des Sciences et Technologies de Lille, Villeneuve d’Ascq, France Abstract (-)-Epigallocatechin (EGC), one of green tea polyphenols, has been shown to inhibit growth of cancer cells. However its mechanism of action is poorly known. We show here that EGC strongly inhibited the growth of breast cancer cell lines (MCF-7 and MDA-MB-231) but not that of normal breast epithelial cells. The inhibition of breast cancer cell growth was due to an induction of apoptosis, without any change in cell cycle progression. MCF-7 cells are known to express a wild-type p53 whereas MDA-MB-231 cells express a mutated p53. The fact that EGC induced apoptosis in both these cell lines suggests that the EGC-triggered apoptosis is independent of p53 status. Moreover, neutralizing antibodies against the death receptor Fas and inhibitors of caspases, such as caspase-8 and -10, efficiently inhibited the EGC-triggered apoptosis. In addition, immunoblotting revealed that EGC treatment was correlated with a decrease in Bcl-2 and an increase in Bax level. These results suggest that EGC-triggered apoptosis in breast cancer cells requires Fas signaling. Breast Cancer Research and Treatment 76 (3): 195-201, December 2002 Remember we are NOT Doctors and have NO medical training. This site is like an Encylopedia - there are many pages, many links on many topics. Support our work with any size DONATION - see left side of any page - for how to donate. You can help raise awareness of CAM.