JNK/MAPK在LPS诱导乳腺癌细胞MCF-7上皮间质转化过程中的作用  

Role of JNK/MAPK in the epithelial- mesenchymal transition of MCF- 7 cells induced by LPS

作　　者：金一[1] 马特[1] 蒋书玲[1] 

机构地区：[1]辽宁省肿瘤医院乳腺外科,辽宁沈阳110000

出　　处：《现代肿瘤医学》2014年第6期1272-1275,共4页Journal of Modern Oncology

基　　金：辽宁省教育厅科学技术研究项目(编号:2009A761);辽宁省科技厅科学技术研究项目(编号:2013022039)

摘　　要：目的:探讨JNK/MAPK在LPS诱导乳腺癌细胞上皮间质转化(EMT)过程中的作用。方法:将乳腺癌细胞MCF-7分为3组:正常对照组、LPS(10μg/ml)处理组、LPS+SP-600125诱导实验组。应用realtime RT-PCR与Western blot法检测上皮细胞表面标志E-钙黏蛋白(E-cadherin)和间质细胞表面标志N-钙黏蛋白(N-cadherin)的表达以及C-Jun氨基末端激酶(JNK)表达。结果:LPS促进乳腺癌细胞系MCF-7的上皮间质转化(EMT)发生。MCF-7细胞的EMT过程伴随JNK1/2活性增加。应用SP-600125(10μmol/L)阻断JNK后,MCF-7细胞的EMT消失。结论:JNK在LPS诱导乳腺癌细胞MCF-7上皮间质转化过程中发挥调控作用。Objective：To discuss the role of JNK/MAPK in the progress of Epithelial-Mesenchymal Transition induced by LPS in MCF -7 cells. Methods：The MCF -7 cells were divided into 3 groups：control group,LPS （ 10μg/ml）treated group and LPS﹢ SP-600125 group. Real-time RT-PCR and Western blot were used to detect the expressions of E-cadherin,N-cadherin and C-Jun N-terminal kinase（ JNK）at mRNA or protein levels. Re-sults：LPS could induce the occurrence of EMT in MCF-7 cells with the activation of JNK1/2;when the SP-600125 was applied,the EMT disappeared. Conclusion：JNK plays a regulatory role in the EMT induced by LPS in MCF-7 cells.

关 键 词：上皮间质转化 乳腺癌细胞MCF-7 脂多糖 C-JUN氨基末端激酶 

分 类 号：R737.9[医药卫生—肿瘤]