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顺铂加重乳腺癌MCF-7细胞D NA损伤促凋亡的研究

袁立明 马楠 曹交欢 文艺 刘向光 周纤纤 匡淑雯 陶晓军 曾赵军

中国药理学通报2017,Vol.33Issue(3):334-337,4.
中国药理学通报2017,Vol.33Issue(3):334-337,4.DOI:10.3969/j.issn.1001-1978.2017.03.009

顺铂加重乳腺癌MCF-7细胞D NA损伤促凋亡的研究

Study of cisplatin aggravating DNA damage and causing a high apoptosis rate on breast cancer MCF-7 cells

袁立明 1马楠 2曹交欢 1文艺 1刘向光 1周纤纤 1匡淑雯 1陶晓军 1曾赵军2

作者信息

  • 1. 湖南师范大学医学院药物工程实验室,湖南长沙 410013
  • 2. 中南大学湘雅医学院分子生物学研究中心,湖南长沙 410078
  • 折叠

摘要

Abstract

Aim Toinvestigatethemechanismsof DNA damage of cisplatin(DDP),a broad spectrum an-ticancer drug on breast cancer MCF-7 cells and to stud-y the mechanism of apoptosis induced by DDP.Meth-ods MCF-7cellsweretreatedbyDDP(0,2,4,6,8, 10 mg·L-1 )for 48 h.MTT assay was used to detect the inhibitory effect of DDP on MCF-7 cells,and IC50 value was calculated.Western blot was adopted to de-tect the expression ofγ-H2AX,which was the marker of DNA double stranded breaks(DSBs)and ATM(sen-sory molecules of DSBs ),the apoptotic signal trans-duction molecule cleaved caspase-3 ,and the proteins associatedwithapoptosis:calpain.Results DDPin-hibited MCF-7 cell activity in a concentration-depend-ent manner and IC50 was 7. 57 mg·L-1 .In contrast to the control group (without DDP treatment),MCF-7 cells with DDP treatment group expressed more γ-H2AX,ATM,cleaved caspase-3 and calpain.Conclu-sions DDPcouldinhibittheactivityofbreastcancer MCF-7 cells.Its mechanisms may be associated with inhibition of MCF-7 cell apoptosis,induction of DNA double strand breaking and the expression of pro-apop-totic protein up-regulating.

关键词

MCF-7细胞/顺铂/DNA损伤/乳腺癌/增殖/凋亡

Key words

MCF-7 cell/cisplatin/DNA damage/breast cancer/proliferation/apoptosis/IC50

分类

医药卫生

引用本文复制引用

袁立明,马楠,曹交欢,文艺,刘向光,周纤纤,匡淑雯,陶晓军,曾赵军..顺铂加重乳腺癌MCF-7细胞D NA损伤促凋亡的研究[J].中国药理学通报,2017,33(3):334-337,4.

基金项目

国家自然科学基金资助项目(No 30600753,81172154) (No 30600753,81172154)

湖南省自然科学基金面上项目(No 2016JJ2088) (No 2016JJ2088)

湖南省教育厅资助项目(No 13C541) (No 13C541)

湖南省中医药管理局资助项目(No 2015123) (No 2015123)

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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