Premium
Epigallocatechin‐3‐gallate and bicalutamide cause growth arrest and apoptosis in NRP‐152 and NRP‐154 prostate epithelial cells
Author(s) -
Morrissey Colm,
Brown Mark,
O'Sullivan Jacintha,
Weathered Natalie,
Watson R. William G.,
Tenniswood Martin
Publication year - 2007
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/j.1442-2042.2007.01774.x
Subject(s) - bicalutamide , apoptosis , medicine , androgen receptor , cell growth , prostate , androgen , growth inhibition , prostate cancer , cancer research , endocrinology , chemistry , cancer , biochemistry , hormone
Aim: A number of epidemiological studies have suggested that consumption of green tea reduces the risk of prostate cancer. The aim of this study was to elucidate the effects of epigallocatechin‐3‐gallate (EGCG), one of the major constituents of green tea, on growth inhibition and apoptosis in prostate epithelial cell lines with and without bicalutamide. Methods: The effects of EGCG and bicalutamide alone and in combination were examined on NRP‐152 and NRP‐154 cells derived from the dorso‐lateral prostate of the Lobund‐Wistar rat. Following treatments, cell number and levels of apoptosis were assessed. Results: After treatment with EGCG, both cell lines displayed a dose‐dependent decrease in cell number; this effect was more pronounced in NRP‐154 cells. This decrease in cell number was caused by growth arrest in NRP‐152 cells and apoptosis in NRP‐154 cells. The apoptotic events in the NRP‐154 cells were concurrent with a loss of manganese superoxide dismutase expression. Androgen ablation was achieved by androgen withdrawal using charcoal stripped serum or treatment with bicalutamide. Bicalutamide decreased cell number and induced apoptosis in a dose‐dependent manner in both cell lines; however, androgen withdrawal did not. There was a loss of androgen receptor expression in NRP‐152 cells with bicalutamide treatment. However, as the NRP‐154 cells are androgen receptor negative, the loss in cell number and increased apoptotic events in these cells cannot be attributed to the anti‐androgenic activity of bicalutamide. Cells treated with a combination of bicalutamide and EGCG also demonstrated a dose‐dependent decrease in cell number that was significantly greater than bicalutamide alone. Conclusions: This study demonstrates the potential use of EGCG and other antioxidants as therapeutic candidates for prostate cancer.