Epigallocatechin-3-gallate and bicalutamide cause growth arrest and apoptosis in NRP-152 and NRP-154 prostate epithelial cells.
OBJECTIVE
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.
Morrissey
Colm
C
Department of Surgery, Mater Misericordiae University Hospital, Conway Institute of Biomolecular and Biomedical Research, Dublin Molecular Medicine Centre, University College Dublin, Dublin, Ireland. cmorriss@u.washington.edu
Brown
Mark
M
O'Sullivan
Jacintha
J
Weathered
Natalie
N
Watson
R William G
RW
Tenniswood
Martin
M
D000813:Anilides / Q000494:pharmacology*; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002452:Cell Count; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D004357:Drug Synergism; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D009570:Nitriles / Q000494:pharmacology*; D011467:Prostate / Q000166:cytology*; D051381:Rats; D017208:Rats, Wistar; D011944:Receptors, Androgen / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D014105:Tosyl Compounds / Q000494:pharmacology*
D000813:Anilides; D000970:Antineoplastic Agents; D000975:Antioxidants; D009570:Nitriles; D011944:Receptors, Androgen; D014105:Tosyl Compounds; D002392:Catechin; C053541:bicalutamide; C045651:epigallocatechin gallate; D013482:Superoxide Dismutase