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作 者:胡卫锋[1] 郭永连[1] 陈琳[1] 李国灏[1] 徐长庚[1] 朱建宁[1] 昌磊[1] 万锋[1]
机构地区:[1]华中科技大学同济医学院附属武汉市中心医院泌尿外科,430014
出 处:《现代泌尿生殖肿瘤杂志》2017年第2期91-94,共4页Journal of Contemporary Urologic and Reproductive Oncology
基 金:武汉市卫计委科研课题(WX13C07)
摘 要:目的探讨17β-雌二醇(E2)联合DNA去甲基化试剂5-氮胞苷(5-AzaC)对雄激素非依赖性前列腺癌22RV1细胞生长抑制和凋亡的影响及作用机制。方法应用17β-E2和/或5-AzaC处理前列腺癌22RV1细胞,并检测细胞生长抑制率、凋亡率以及雌激素受体2(ESR2)和p75神经生长因子受体(p75NTR)的表达情况。结果 17β-E2或5-AzaC呈时间及浓度依赖性抑制22RV1细胞增殖,17β-E2和5-AzaC 48hIC50分别是0.2μmol/L和4.0μmol/L。17β-E2(0.2μmol/L)+5-AzaC(4.0μmol/L)对22RV1细胞的增殖抑制及凋亡表现出协同作用,17β-E2或5-AzaC均能上调ESR2和p75NTR的mRNA及蛋白的表达,且联合应用时效果更明显。结论联合应用17β-E2和5-AzaC上调ESR2和p75NTR的表达可能是雄激素非依赖性前列腺癌治疗的一个潜在的治疗策略。Objective To investigate the effects of 17β-estradiol combined with 5-AzaC on pro- liferation inhibition and apoptosis of human androgen-independent prostate carcinoma cell line 22RV1 and its mechanism. Methods After 22RV1 were treated with 17β-estradiol and the DNA demethyl- ation reagent 5-AzaC, the proliferation inhibition rates and apoptosis percentage of cell were meas- ured, the expression of estrogen receptor (ESR) subtype 2 and p75NTR were detected. Results A time - and dose- dependent proliferation inhibition of 17β-estradiol or 5-AzaC was demonstrated in 22RV1. The IC50 values of 17μ-estradiol and 5-AzaC on 48 h were 0.2 μmol/L and 4.0 μmol/L respectively. After treated 22RV1 by the combined 17lbestradiol and 5-AzaC, the proliferation inhibi- tion and apoptosis of 22RV1 cells showed a synergistic activity. The expression of ESR2 and p75NTR in 22RV1 were upregulated after treated 17β-estradiol or 5-AzaC, whatmore the combined effect was more obvious. Conclusions The up-regulation of ESR2 and p75NTR by 17β-estradiol plus 5-AzaC may be a potential therapeutic strategy for the treatment of androgen refractory prostate cancer.
关 键 词:雄激素非依赖性前列腺癌 17Β-雌二醇 5-氮胞苷 P75NTR
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