谭波宇,韦鸿雁,陈 丽.人血白蛋白增强顺铂对MCF7细胞的耐药作用[J].中国肿瘤,2018,27(4):316-320.
人血白蛋白增强顺铂对MCF7细胞的耐药作用
Human Albumin Enhances Cisplatin Resistance to MCF7 Cells
投稿时间:2017-07-24  
DOI:10.11735/j.issn.1004-0242.2018.04.A013
中文关键词:  人血清白蛋白  顺铂  耐药  MCF7  ERCC1
英文关键词:human serum albumin  cisplatin  drug resistance  MCF7  ERCC1
基金项目:湖南省药学会科研资助项目生物专项 (xy2015007)
作者单位
谭波宇 湖南师范大学附属第一医院湖南省人民医院药学部 
韦鸿雁 湖南师范大学附属第一医院湖南省人民医院药学部 
陈 丽 湖南师范大学附属第一医院湖南省人民医院药学部 
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中文摘要:
      摘 要:[目的] 探讨人血清白蛋白(HSA) 联用顺铂 (DDP) 对MCF7细胞耐药的影响。[方法] 不同浓度DDP干预MCF7 细胞 72h,CCK8 检验细胞增殖抑制率。选用DDP的IC50浓度分别与10、20μmol/L HSA联用,进一步检测联合用药对 MCF7细胞的增殖抑制率。样品分为空白对照组、顺铂组、HSA组、顺铂联合HSA治疗组(10或20μmol/L)。各组处理MCF7细胞72h,实时荧光定量PCR (qRT-PCR)和免疫印迹法检测ERCC1 mRNA和蛋白表达。 [结果] DDP联用10或20μmol/L HSA 对MCF7 的增殖抑制率分别为(50.97±1.50)%、(45.15±2.10)%,单独用药组DDP对MCF7 的增殖抑制率为(55.60±5.20)%。qRT-PCR和Western blot检测表明DDP联用HSA (20μmol/L) 显著增强ERCC1 mRNA和蛋白的表达。[结论] DDP联合使用高浓度HSA可通过上调ERCC1表达诱导化疗药物耐药。
英文摘要:
      Abstract:[Purpose] To investigate the effect of human serum albumin(HSA)combined with cisplatin(DDP)on the resistance of MCF7 cells. [Methods] MCF7 cells were intervened with DDP at different concentrations,and the inhibition rate of cell proliferation was examined by CCK8 after 72h treatment. The IC50 concentration of DDP was selected to be combined with 10 or 20μmol/L HSA respectively,and the inhibition rate of MCF7 cell proliferation by combined administration was further detected. The samples were divided into blank control group,DDP group,HSA group,DDP combined with HAS(10 or 20μmol/L)treatment group. Each group treated MCF7 cells for 72h and the expression of ERCC1 were detected by real-time quantitative PCR(qRT-PCR)and Western blot. [Results] DDP combined with 10 or 20 umol/L HSA on MCF7 proliferation inhibition rate were(50.97±1.50)% and(45.15±2.10)% respectively. The inhibition rate of DDP alone was(55.60±5.20)%. qRT-PCR and Western blot assays showed that DDP combined with HSA(20μmol/L)significantly enhanced ERCC1 mRNA and protein expression. [Conclusion] DDP combined with high concentration of HSA can induce resistance to chemotherapeutic drugs by up-regulation of ERCC1 expression.
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