三氧化二砷抑制乳腺癌MCF-7细胞作用机制的研究  

Mechanism underlying MCF-7 cell inhibitory effect induced by arsenic trioxide

作　　者：王莹[1] 郝艳坤[1] 安佰柱[1] 王羽[1] 

机构地区：[1]牡丹江医学院,黑龙江牡丹江157011

出　　处：《现代肿瘤医学》2014年第11期2542-2544,共3页Journal of Modern Oncology

基　　金：黑龙江省卫生厅科研课题(编号:2011-323);牡丹江医学院科学技术研究项目(编号:2011-07)

摘　　要：目的:探讨三氧化二砷(As2O3)抑制乳腺癌MCF-7细胞的作用机制。方法:噻唑兰(MTT)法检测As2O3对MCF-7细胞存活率的影响;流式细胞技术检测As2O3引起MCF-7细胞凋亡。通过caspas-3试剂盒检测其活性,推测其可能的凋亡信号通路。结果:MTT实验表明As2O3使MCF-7细胞存活率下降并呈现剂量依赖的量效关系;流式细胞测定结果证实As2O3对乳腺癌细胞具有致凋亡作用;As2O3作用后的MCF-7细胞caspase-3的活性显著增高。结论:As2O3诱导MCF-7细胞凋亡,其机制至少部分与激活caspase-3有关。Objective：To explore the mechanism of inhibitory effect induced by arsenic trioxide （As2O3） in human breast cancer MCF-7 cells.Methods：The effect of As2O3 on cell viability was assayed by methylthiazoletetrazolium （MTT）.Apoptosis was analyzed by flow cytometry.Caspase-3 activity was detected by caspase assay kit to speculate the possible apoptotic signaling pathway.Results：MTT result showed As2O3 reduced the viability of MCF-7 cells in a concentration-dependent manner.Flow cytometry assay confirmed apoptosis result in As2O3-treated MCF-7 cells.The activity of caspase-3 increased in As2O3-treated group compared with control group.Conclusion：As2O3 induces apoptosis of MCF-7 cells,caspase-3 activation at least is involved in this process.

关 键 词：三氧化二砷 MCF-7细胞 凋亡 CASPASE-3 

分 类 号：R73-361[医药卫生—肿瘤] R737.9[医药卫生—临床医学]