乳腺癌耐药性与MAPK信号转导关系的研究  

The Relationship between p38 MAPK Pathway and Adriamycin Resistance of Breast Carcinoma MCF-7/Adr Cells

作　　者：崔文[1] 孔灵玲[1] 肖兰[2] 王旭[1] 张国安[1] 姜晓刚[1] 魏红[1] 

机构地区：[1]济宁医学院病理学教研室 [2]中山大学附属第三医院妇产科博士后流动站

出　　处：《济宁医学院学报》2008年第4期273-275,共3页Journal of Jining Medical University

基　　金：山东省教育厅课题(No.Y07YD17);卫生厅十一五医药科技卫生计划(No.2007HZ018)资助

摘　　要：目的探讨乳腺癌细胞阿霉素耐药性与p38MAPK通路的关系。方法用流式细胞术检测SB203580(15μmol/L)干预后细胞的凋亡、细胞内阿霉素浓度的改变、细胞对阿霉素敏感性。结果经SB203580(15μmol/L)干预24h和48h后,流式细胞仪检测见MCF-7/Adr细胞发生显著凋亡,凋亡率分别为25.36±1.17%和38.21±1.25%,并呈一定时间依赖性(P<0.05);显著高于空白对照组及DMSO组MCF-7/Adr细胞的0.65±0.21%和0.81±0.16%(P<0.01);细胞内阿霉素浓度亦显著增加,平均荧光强度分别为32.45±2.36及41.66±3.12,均显著高于空白对照组及DMSO组的14.17±1.45及16.28±0.63(P<0.01);另外,SB203580干预48h使MCF-7/Adr细胞内阿霉素浓度增加的作用强于24h组,两者间差异有统计学意义(P<0.05)。结论提示p38MAPK通路与乳腺癌细胞阿霉素耐药密切相关。Objective To investigate the relationship between p38MAPK pathway and the adriamycin resistance of breast carcinoma ceils. Methods Using p38MAPK inhibitor SB203580 to analyze the effect on the cell apoptosis through FITC - Annexin - V/PI double staining. The concentration of adriamycin was detected by the flow cytometry （FCM）. Results After intervening with SB203580 for 24 hours and 48 hours the apoptosis efficiency was increased remarkably. They were much higher in 24h group （25.36 ± 1.17）% and 48h group （38.21 ± 1. 25 ） % ） than in control group （ 0.65 ±0. 21 ） % and DMSO group （0.81 ±0. 16） % （ P 〈0.01 ）. And the cell apoptosis efficiency increased in a time- dependent manner （P 〈0.05 ）; Inhibition of p38MAPK pathway could increase cellular adriamycin accumulation： It was higher in 24h group （32.45 ±2.36） and 48h group （41.66 ±3. 12） than in control group （14.17 ±1.45） and DMSO group （16.28±0.63） （P〈0.01）.Conclusion Therehas a closely relationship between p38MAPK pathway and the adriamycin resistance of breast carcinoma cells.

关 键 词：乳腺癌 P38MAPK通路 阿霉素耐药 

分 类 号：R737.9[医药卫生—肿瘤] R818.023[医药卫生—临床医学]