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

Journal Article · Fri Mar 23 04:00:00 EDT 2007 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/j.bbrc.2007.01.003· OSTI ID:20979835

Jie, Qin ^[1]; Liping, Xie ^[1]; Xiangyi, Zheng ^[1]; Yunbin, Wang ^[1]; Yu, Bai ^[1]; Huafeng, Shen ^[1]; Longcheng, Li ^[2]; Dahiya, Rajvir ^[2]

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1. Department of Urology, First Affiliated Hospital, Medical College, Zhejiang University, Qingchun Road 79, Hangzhou 310003, Zhejiang Province (China)
2. 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, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 4 Vol. 354; ISSN 0006-291X; ISSN BBRCA9
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
APOPTOSIS
BEVERAGES
BLADDER
BORON CHLORIDES
CELL PROLIFERATION
GALLIUM COMPOUNDS
HUMAN POPULATIONS
INHIBITION
MITES
MODULATION
NEOPLASMS
OXYGEN COMPOUNDS
PROTEINS
RADIATION DOSES
TIME DEPENDENCE