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Pgp、MRP1和GST介导乳腺癌细胞对As_2O_3耐药的初步研究 被引量:4

A preliminary study of breast cancer cells' tolerance to arsenic trioxide mediated by Pgp,MRP1 and GST
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摘要 目的探讨乳腺癌细胞对三氧化二砷(As2O3)是否耐药及其机制。方法以乳腺癌MCF-7/ADR和MCF-7细胞为研究对象,通过MTT还原法比较As2O3对二者细胞毒作用的差异,用SABC法测定细胞用药前后P糖蛋白(Pgp)、多药耐药相关蛋白(MRP1)的表达;用紫外分光光度计法测定细胞谷胱甘肽S转移酶(GST)的活性。结果MCF-7/ADR和MCF-7细胞对As2O3的敏感性存在显著差异,IC50值分别为12.8μmol/L、3.0μmol/L,表明MCF-7/ADR细胞对As2O3耐药;MCF-7/ADR细胞Pgp、MRP1和GST的表达用药前已明显强于MCF-7细胞,并在用药后呈过度共表达,而后者未出现此情况。结论Pgp、MRP1和GST的表达增强介导了乳腺癌MCF-7/ADR细胞对As2O3耐药。 Objective To explore whether human breast cancer cells are resistant to arsenic trioxide and to study associated mechanism in vitro. Methods MTT test was used to detect the sensibitity of human breast cancer MCF -7 and muhidrug resistant MCF-7/ADR cell line to arsenic trioxide. The expression of Pglycoprotein (Pgp) and muhidrug resistance associaled prolein(MRP) of the two cell lines were assaied by SABC immunohistochemical method before and after medication.and the glutamylcysteinyl glycine sulfurlransferase (GST)activity was detected by uhraviolet spectrophotometer method. Results The sensibility of MCF- 7 and MCF-7/ADR cell to arsenic trioxide was not consistent,and the IC50 was 3. 0μmol/L and 12. 8μmol/L respcetivly. Meanwhile, marked overexpression of Pgp, MRP and GST of MCF-7/ADR cell after medication were detected, but it did not occur in MCF -7 cell. Conclusion Overexpression of Pgp, MRP1 and GST contributes to the resistance of muhidrug resislance MCF-7/ADR cell to arsenic trioxide.
出处 《重庆医学》 CAS CSCD 北大核心 2010年第7期812-814,共3页 Chongqing medicine
关键词 乳腺癌 多药耐药 arsenic trioxide breast carcinoma muhidrug resistance
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参考文献6

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