Morrissey Colm, Brown Mark, O'Sullivan Jacintha, Weathered Natalie, Watson R William G, Tenniswood Martin
Department of Surgery, Mater Misericordiae University Hospital, Conway Institute of Biomolecular and Biomedical Research, Dublin Molecular Medicine Centre, University College Dublin, Dublin, Ireland.
Int J Urol. 2007 Jun;14(6):545-51. doi: 10.1111/j.1442-2042.2007.01774.x.
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.
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.
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.
This study demonstrates the potential use of EGCG and other antioxidants as therapeutic candidates for prostate cancer.
多项流行病学研究表明，饮用绿茶可降低前列腺癌风险。本研究旨在阐明绿茶的主要成分之一表没食子儿茶素-3-没食子酸酯（EGCG）对有无比卡鲁胺的前列腺上皮细胞系生长抑制和凋亡的影响。
研究了EGCG和比卡鲁胺单独及联合使用对源自Lobund-Wistar大鼠背外侧前列腺的NRP-152和NRP-154细胞的影响。处理后，评估细胞数量和凋亡水平。
用EGCG处理后，两种细胞系的细胞数量均呈剂量依赖性减少；这种作用在NRP-154细胞中更明显。细胞数量的减少是由NRP-152细胞的生长停滞和NRP-154细胞的凋亡引起的。NRP-154细胞中的凋亡事件与锰超氧化物歧化酶表达的丧失同时发生。通过使用活性炭处理的血清撤去雄激素或用比卡鲁胺治疗实现雄激素去除。比卡鲁胺在两种细胞系中均以剂量依赖性方式减少细胞数量并诱导凋亡；然而，撤去雄激素则没有这种作用。比卡鲁胺处理的NRP-152细胞中雄激素受体表达丧失。然而，由于NRP-154细胞为雄激素受体阴性，这些细胞中细胞数量的减少和凋亡事件的增加不能归因于比卡鲁胺的抗雄激素活性。用比卡鲁胺和EGCG联合处理的细胞也显示出细胞数量呈剂量依赖性减少，且明显大于单独使用比卡鲁胺。
本研究证明了EGCG和其他抗氧化剂作为前列腺癌治疗候选药物的潜在用途。
