摘要
目的:研究三氧化二砷(As2O3)对人鼻咽癌CNE2Z细胞的生物学效应及其作用机制。方法:台盼蓝计数法计算As2O3的IC50;CNE-2Z细胞经As2O3处理后,通过流式细胞仪、荧光染色及DNA电泳检测细胞凋亡;流式细胞仪测定bcl2和bax阳性细胞百分率;罗丹明123染色后进行线粒体膜电位分析。结果:As2O3在一定浓度范围内以浓度依赖的方式抑制CNE2Z细胞生长,其IC50为(1.35±0.30)μmol/L;0.5~2.0μmol/LAs2O3处理CNE2Z细胞后,流式细胞仪检测出凋亡峰,荧光显微镜下可见明显的细胞凋亡形态特征,琼脂糖凝胶电泳出现DNA梯形条带;As2O3对bcl2的表达没有影响(P>0.05),但能显著增加bax的表达(P<0.01)及降低线粒体膜电位(P<0.01)。结论:As2O3在体外可诱导鼻咽癌CNE2Z细胞凋亡,其机制可能与上调bax表达和降低线粒体膜电位有关。
Objective:To investigate the pos sibility and t he mechanism of human nasopharyngeal carcinoma (NPC)CNE-2Z ce ll apoptosis induced by ars enic trioxide(As 2 O 3 ).Methods :The cytotoxic activity of As 2 O 3 was quantified by determining IC 50 in CNE-2Z cells using trypan blue exc lusion.After treatment with As 2 O 3 ,apoptotic cells were detected with flow cytometry,fluorescence stain ing and DNA electrophoresis;the inf luence of As 2 O 3 on bcl-2and Bax expression was observed with flow cytometry;the ch ange o f mitochondrial membrane pote ntial(ΔΨm)was analyzed with flow cytometry aft er Rhodamine123staining.Results:As 2 O 3 inhibited the growth of CNE-2Z cells in a dose-dependent manner in a cert a in range of dose with a IC 50 of 1.35±0.30μmol /L;Apoptotic peak,characteristic morphologic f eatures of apoptosis and DNA ladder were observed in CNE-2Z cells treated with 0.5-2.0μmol /L As 2 O 3 ;After treatment with 2.0μmol /L As 2 O 3 ,no change of Bcl-2protein level was observed(P>0.05),while Bax w as up-regulated signifi cantly(P<0.01)and a significant loss ofΔΨm wa s detected(P<0.01).Conclusions :As 2 O 3 may induce apoptosis of NPC CNE-2Z cells,and its mechanism is related to the up-regulation of Bax and loss ofΔΨm.
出处
《癌症》
SCIE
CAS
CSCD
北大核心
2001年第10期1061-1064,共4页
Chinese Journal of Cancer
基金
广东省重点学科经费资助项目(编号9906)