[1]曾少波,兰明银,菅志远,等.乳腺癌细胞耐药过程中p38MAPK活性与细胞凋亡的关系[J].中华乳腺病杂志(电子版),2009,3(1):46.
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乳腺癌细胞耐药过程中p38MAPK活性与细胞凋亡的关系()

中华乳腺病杂志(电子版)[ISSN:1674-0807/CN:11-9146/R]

卷:
第3卷
期数:
2009年1期
页码:
46
栏目:
实验研究
出版日期:
2009-02-01

文章信息/Info

作者:
曾少波;兰明银;菅志远;李恒;严斌;张敏;周猛;江斌
郧阳医学院太和医院普外科
关键词:
乳腺癌细胞凋亡p38MAPK多药耐药
摘要:
目的 研究乳腺癌细胞耐药过程中p38MAPK活性与细胞凋亡的关系,探讨p38MAPK信号转导途径在其中的作用。方法 以p38MAPK特异性抑制剂SB203580处理乳腺癌耐药细胞MCF-7/ADM,采用流式细胞技术分析对细胞凋亡的影响;MTT检测MCF-7/ADM细胞对阿霉素的半数药物抑制浓度(IC50);Westernblot检测SB203580处理MCF-7/ADM和MCF-7两株细胞后p38MAPK蛋白表达水平;RT-PCR检测细胞内MDR-1 mRNA水平。结果 SB203580(10μmol/L)干预24h后MCF-7/ADM细胞的凋亡率为(26.73±4.90)%,与未干预组和对照组凋亡率相比差异有显著统计学意义(F=143.80,P<0.001);MCF-7/ADM细胞对阿霉素的敏感性明显提高(F=148927.10,P<0.001),相对逆转率达68.45%;与对照组和未干预组相比,干预组的MDR1 mRNA(F=9139.24,P<0.001)及p38MAPK(F=685.42,P<0.001)蛋白表达水平明显降低。结论 p38MAPK信号转导途径与乳腺癌耐药密切相关,其可能机制为p38MAPK保护人乳腺癌耐药细胞(MCF-7/ADM)逃避凋亡,阻断该通路可增强乳腺癌耐药细胞发生凋亡。

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更新日期/Last Update: 2009-01-20