A component of green tea (-)-epigallocatechin-3-gallate, promotes apoptosis in T24 human bladder cancer cells via modulation of the PI3K/Akt pathway and Bcl-2 family proteins
- Department of Urology, First Affiliated Hospital, Medical College, Zhejiang University, Qingchun Road 79, Hangzhou 310003, Zhejiang Province (China)
- Department of Urology, University of California San Francisco and Veteran Affairs Medical Center San Francisco, San Francisco, CA (United States)
Bladder cancer is the fourth most common cancer in men and ninth most common in women. It has a protracted course of progression and is thus an ideal candidate for chemoprevention strategies and trials. This study was conducted to evaluate the chemopreventive/antiproliferative potential of (-)-epigallocatechin gallate (EGCG, the major phytochemical in green tea) against bladder cancer and its mechanism of action. Using the T24 human bladder cancer cell line, we found that EGCG treatment caused dose- and time-dependent inhibition of cellular proliferation and cell viability, and induced apoptosis. Mechanistically, EGCG inhibits phosphatidylinositol 3'-kinase/Akt activation that, in turn, results in modulation of Bcl-2 family proteins, leading to enhanced apoptosis of T24 cells. These findings suggest that EGCG may be an important chemoprevention agent for the management of bladder cancer.
- OSTI ID:
- 20979835
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 354, Issue 4; Other Information: DOI: 10.1016/j.bbrc.2007.01.003; PII: S0006-291X(07)00031-9; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
Similar Records
Epigallocatechin-3-gallate (EGCG) protects against chromate-induced toxicity in vitro
Green tea polyphenol epigallocatechin-3-gallate differentially modulates oxidative stress in PC12 cell compartments