As2O3诱导人卵巢癌细胞株HO8910凋亡和端粒酶活性的关系

目的探讨As2O3诱导HO8910细胞凋亡和端粒酶活性变化的关系。方法用不同浓度的As2O3溶液作用卵巢癌细胞株HO8910,于不同时间点收集细胞,MTT法检测细胞生长抑制率;FCM检测细胞凋亡率;TRAP-银染法观察端粒酶活性的变化。结果As2O3溶液对HO8910有生长抑制和诱导凋亡的作用,与药物浓度和作用时间相关。不同浓度As2O3作用HO8910细胞,其端粒酶活性在24h无明显改变,随着作用时间的延长,端粒酶活性逐渐下降,随着药物浓度的升高端粒酶活性也呈不断下降趋势,以致消失。结论As2O3可以诱导卵巢癌细胞株HO8910发生凋亡,其机制可能不是通过端粒酶活性下降直接调控的,但端粒酶调控与凋亡调控有一定相关性。

Relationship between telomerase activity and apoptosis induced by arsenic trioxide in ovarian carcinoma cell line HO8910

Objective To explore the relationship between the variation of telomerase activity and apoptosis by arsenic trioxide in ovarian carcinoma cell line HO8910.Methods We collected HO8910 cells at 24 h,48 h and 72 h respectively under different concentrations of As2O3.The inhibition rates of cells were determined by methyl thiazolyl tetrazolium (MTT) assay to evaluate the effect of As2O3.The percentage of apoptosis was detected by flow cytometry (FCM).Telomerase activity of ovarian carcinoma cells was determined by the method of TRAP-PAGE argentation.Results Growth inhibition and apoptosis induction were evoked by different concentrations of As2O3 in HO8910 cells in a time- and concentration-dependent manner.Within 24 h,the telomerase activity of HO8910 cells had no obvious change in different concentrations of As2O3.The telomerase activity gradually decreased till vanished with the prolongation of time and increase of concentrations.Conclusion As2O3 can induce HO8910 cells apoptosis.Apoptosis induced by arsenic trioxide may not be directly regulated through the decrease of telomerase activity.However,correlation exists between telomerase and apoptosis regulation.