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大黄素下调ERCC1蛋白表达逆转乳腺癌化疗耐药的机制研究
引用本文:丘禹洪,周颉,刘昱磊,谢建生. 大黄素下调ERCC1蛋白表达逆转乳腺癌化疗耐药的机制研究[J]. 深圳中西医结合杂志, 2012, 22(4): 226-229
作者姓名:丘禹洪  周颉  刘昱磊  谢建生
作者单位:南方医科大学附属深圳妇幼保健院,广东深圳,518048
摘    要:目的:探讨中药大黄素下调ERCC1蛋白表达与其逆转乳腺癌MCF-7/Adr细胞株多药耐药的相互关系,阐明大黄素逆转细胞耐药与ERCC1的作用机制。方法:采用MTT比色法对乳腺癌耐药细胞株MCF-7/Adr及敏感细胞株MCF-7进行药敏试验,蛋白质印迹法检测细胞中ERCC1蛋白的表达。结果:MCF-7/Adr对阿霉素和顺铂的耐药倍数分别为21和11倍,在加入10g/mL大黄素后,耐药逆转倍数分别为2.86和1.79。MCF-7/Adr分别经10g/mL和20g/mL大黄素处理后第2、4、6、10天ERCC1蛋白的表达水平逐渐降低,大黄素20g/mL浓度下作用更明显。结论:大黄素可以通过下调ERCC1的表达水平而逆转MCF-7/Adr细胞多药耐药,并与大黄素的浓度和作用时间有一定的相关性。

关 键 词:大黄素  乳腺肿瘤  多药耐药  ERCC1

Mechanism of Emodin Down-regulate ERCC1 Protein Expression Reversed Chemotherapy Resistance in Breast Cancer
QIU Yu-hong , ZHOU Jie , LIU Yu-lei , XIE Jian-sheng. Mechanism of Emodin Down-regulate ERCC1 Protein Expression Reversed Chemotherapy Resistance in Breast Cancer[J]. Shenzhen Journal of Integrated Traditional Chinese and Western Medicine, 2012, 22(4): 226-229
Authors:QIU Yu-hong    ZHOU Jie    LIU Yu-lei    XIE Jian-sheng
Affiliation:(Shenzhen Maternity and Child Healthcare Hospital,Southern Medical University,Guangdong Shenzhen 518048)
Abstract:Objective To investigate the reversal effect of emodin,which was a traditional Chinese medicine,on multi-drug resistant breast cancer cell line MCF-7/Adr and explore its influence on the expression of ERCC1.Methods MTT assay was used for drug sensitivity tests and Western Blot for ERCC1 protein.Results The resistance multiples of adriamycin and cisplatin were 21 and 11 in MCF-7/Adr,the reversal multiples of drug resistance were 2.86 and 1.79 respectively after added emodin(10 g/mL).MCF-7/Adr cells treated with two concentrations(10 g/mL,20 g/mL) of emodin,after 2,4,6,10 days,the trend of ERCC1 expression was gradually downward,it was more obvious comparatively at the concentration of 20 g/mL.Conclusion Emodin can reverse the multi-drug resistance on MCF-7/Adr cells,and can down-regulate the expression of ERCC1 protein in a time-dependent manner.
Keywords:Emodin  Breast neop lasm  Multi-drug resistance  Excision repair cross complementation group 1
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