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全反式维甲酸对前列腺癌PC-3细胞Bcl-2、Bax表达的影响
引用本文:王恒兵,严春寅,陈卫国.全反式维甲酸对前列腺癌PC-3细胞Bcl-2、Bax表达的影响[J].苏州大学学报(自然科学版),2006,26(3):447-449,463.
作者姓名:王恒兵  严春寅  陈卫国
作者单位:苏州大学附属第一医院泌尿外科,江苏苏州215006
摘    要:目的 探讨全反式维甲酸(ATRA)对人雄激素非依赖性前列腺癌细胞株PC-3增殖的抑制作用及其Bel-2和Bax表达的影响。方法以不同浓度的ATRA处理PC-3细胞,甲基偶氮唑蓝(MTT)比色法检测细胞增殖抑制情况;流式细胞仪和免疫细胞化学法检测PC-3细胞Bax和Bcl-2的表达。结果ATRA浓度为(10^-6~10^-4)mol/L时,可明显抑制PC-3细胞的增殖(P〈0.01),并具有时间-剂量依赖性。ATRA处理后PC-3细胞Bcl-2表达下调,Bax表达上调。随ATRA浓度增加,Bcl-2/Bax的比值不同程度地下降(P〈0.05)。结论ATRA对PC-3细胞具有明显的增殖抑制作用,并且与ATRA下调Bcl-2表达、上调Bax表达有关。

关 键 词:全反式维甲酸  前列腺癌  细胞凋亡
文章编号:1673-0399(2006)03-0447-03
收稿时间:2005-08-24
修稿时间:2005-08-24

Effects of All-trans-retinoic Acid on the Expression of Bcl-2 and Bax in Human Prostate Cancer PC-3 Cell Line
WANG Heng-bing,YAN Chun-yin,CHEN Wei-guo.Effects of All-trans-retinoic Acid on the Expression of Bcl-2 and Bax in Human Prostate Cancer PC-3 Cell Line[J].Suzhou University Journal of Medical Science,2006,26(3):447-449,463.
Authors:WANG Heng-bing  YAN Chun-yin  CHEN Wei-guo
Institution:Dept of Urology, the First Hospital Affiliated to Suzhou University, Jiangsu Suzhou 215006, China
Abstract:Objective To investigate the effects of all-transretinoic acid(ATRA) on the proliferation and the expression of Bcl-2 and Bax in human androgen-independent prostate cancer PC-3 cell line.Methods Human prostate cancer PC-3 cell line was cultured in medium containing in different of ATRA concentrations.Cell proliferating inhibition was tested by MTT assay.Flow cytometry and immunocytochemistry were used to analyze the expression of Bcl-2 and Bax in PC-3 cells.Results (ATRA) inhibited PC-3 cell proliferation in a dose-dependent and time-dependent manner(P<0.01).(ATRA) down-regulated the expression of Bcl-2 and up-regulated the expression of Bax in PC-3 cells.With the increase of ATRA concentration,the ratio of Bcl-2 to Bax decreased gradually.Conclusion ATRA can significantly inhibit the proliferation of PC-3 cells.And it is related with down-regulation of the expression of Bcl-2 and up-regulation of the expression of Bax.
Keywords:Bcl-2  Bax
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