三氧化二砷对人肺癌细胞株增殖和凋亡的影响  

Cell cycle arrest and apoptosis induced by arsenic trioxide in human lung cancer cell line

作　　者：董继华[1] 吴裕丹[1] 董晓荣 许林锋[1] 刘莉[1] 

机构地区：[1]同济医科大学附属协和医院中心实验室,武汉430022

出　　处：《中国肺癌杂志》2000年第6期435-437,共3页Chinese Journal of Lung Cancer

摘　　要：目的　探讨三氧化二砷 (As2 O3 )对人肺癌的潜在性治疗作用及可能的机制。方法　选用人肺癌细胞株GLC 82 ,运用细胞培养法、MTT法、流式细胞术 (FCM)检测细胞生长曲线、细胞增殖、细胞周期和细胞凋亡。结果　三氧化二砷可明显抑制GLC 82细胞的增殖 ,其抑制作用具有时—效和量—效关系。当 4.0 μmol/L三氧化二砷处理GLC 82细胞 96小时 ,增殖抑制率达 81.0 5 %。FCM检测肿瘤细胞DNA含量 ,观察到三氧化二砷使GLC 82细胞周期阻滞于G2 /M期 ,细胞周期进程变慢 ,同时出现剂量依赖性亚G1峰。结论　三氧化二砷能有效地抑制人肺癌细胞株GLC 82的增殖 ,其可能的机制与三氧化二砷使细胞阻滞于G2 /M期并诱导其凋亡有关。Objective To explore the potential therapeutic effect of arsenic trioxide(As 2O 3)on human lung cancer. Methods Cell growth curves, cell proliferation, cell cycle and apoptosis of human lung cancer cell line GLC 82 were detected by the MTT method and flowcytometry (FCM). Results The data showed that As 2O 3 significantly inhibited proliferation of GLC 82 cells and the inhibiting effects had a dose and time dependence. The cell proliferation inhibition rate was 81.05% when treated with 4.0?μmol/L As 2O 3 for 96 hours. The change of DNA content of GLC 82 cells indicated that As 2O 3 was able to block cell cycle progress in G2/M phase, with appearance of sub G1 peak in a dose dependent manner. Conclusion As 2O 3 can effectively inhibit the proliferation of human lung cancer cell line GLC 82 and the possible mechanisms may be related to G2/M phase arrest and apoptosis induced by As 2O 3.

关 键 词：三氧化二砷 肺癌 GLC-82细胞 凋亡 治疗 机制 

分 类 号：R734.2[医药卫生—肿瘤]