解剖学报

›› 2007, Vol. 38 ›› Issue (1): 43-46.doi:

• 论著 • 上一篇    下一篇

17β-雌二醇逆转乳腺癌耐药蛋白介导的多药耐药机制

李文通1;周庚寅1*;宋现让2;迟伟玲3;魏玲2;王兴武2;张晓芳1   

  1. 1. 山东大学医学院病理学教研室，济南 250012；2. 山东省肿瘤医院基础研究中心，济南 250117； 3. 山东大学医学院分子生物学教研室，济南 250012
  • 收稿日期:2005-08-10 修回日期:2006-08-06 出版日期:2007-02-06
  • 通讯作者: 周庚寅

THE STUDY OF THE MECHANISM OF 17βESTRADIOL ON REVERSAL OF THE BREAST CANCER RESISTANT PROTEIN-MEDIATED MULTIDRUG RESISTANCE

  1. 1. Department of Pathology, Medical School, Shandong University, Ji′nan 250012, China; 2. Department of Cancer Research Center, Shandong Tumor Hospital and Institute, Ji′nan 250117, China; 3. Department of Biochemistry and Molecular Biology, Medical School, Shandong University, Ji′nan 250012, China
  • Received:2005-08-10 Revised:2006-08-06 Online:2007-02-06
  • Contact: ZHOU Geng-yin

关键词: 雌激素, 乳腺癌耐药蛋白, 基因调控, 启动子, 耐药逆转

Abstract: Objective To explore the mechanism of the reversal of breast cancer resistant protein-mediated multidrug resistance by 17βestradiol. Methods Two BCRP expressing cell lines of MCF-7/MX20 and MCF-7/BCRP were established in which breast canrcer resistant protein(BCRP) was promoted by BCRP promoter and cytomegalovirus(CMV) promoter respectively.These drug resistant cell lines were cultured in medium containing 17βestradiol. Fourtyeight hours later,cytotoxicity assay,mitoxantrone efflux assays,quantitative RT-PCR were performed to observe the reversal function of BCRP by 17βestradiol on MCF-7/MX20 and MCF-7/BCRP respectively. Results After being treated with 17βestradiol,the intensity of mitoxantrone in MCF-7/BCRP was weaker than that in MCF-7/MX20 and the BCRP mRNA level in MCF-7/BCRP was high than that in MCF-7/MX20.The results of these experiments revealed that 17βestradiol could reverse the BCRP mediated multidrug resistance(MDR) in MCF-7/M

Key words: Estrogen, Breast cancer resistant protein, Gene regulation, Promoter

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