ERK／p-38MAPK信号通路在乳腺癌骨转移中的作用  

Effects of ERK/p-38 MAPK signal pathway in migration and invasion of breast cancer cells

作　　者：赵凯[1] 赵茜[1] 谭群亚[1] 杨翀[1] 王玮[1] 董兵[1] 苏燕燕[1] 

机构地区：[1]浙江省中西医结合医院外三科,杭州310003

出　　处：《浙江医学》2012年第21期1735-1738,共4页Zhejiang Medical Journal

基　　金：杭州市医药卫生科技计划资助项目（2008A015）;浙江省医药卫生科技计划资助项目（2011KYA138）

摘　　要：目的研究胞外信号调节激酶（ERK）和 p-38丝裂原活化蛋白激酶（MAPK）信号通路在乳腺癌骨转移中的作用.方法用 ERK/p-38MAPK 抑制剂（UO126和 SB202190）处理人可溶性核因子κB 受体活化因子配体（shRANKL）诱导的乳腺癌细胞 MDA-MB-231后,以 Western 印迹法检测细胞中 p-ERK 和 p-MAPK 蛋白水平变化,细胞划痕和 Transwel 实验研究细胞迁移和侵袭.结果 shRANKL 诱导细胞24 h 后,细胞迁移和侵袭能力、细胞内 p-ERK 和 p-p38MAPK 蛋白表达均显著性增加.然而,ERK/MAPK 蛋白抑制剂和 shRANKL 联合使用显著性降低 shRANKL 诱导的迁移和侵袭能力.结论抑制 ERK/p-38MAPK信号通路降低乳腺癌细胞转移.Objective To investigate the effect of ERK/p-38 MAPK signal pathway in the migration and invasion of breast cancer cells. Methods Breast cancer MDA-MB-231 cells were treated with shRANKL, then incubated with ERK and p-38MAPK inhibitors UO126 and SB202190, the expression of p-ERK and p-MAPK proteins was determined by Western blot; cell migration and invasion were examined by scratch wound assay and Transwell methods, respectively. Results Cell migration and invasion was enhanced, and the expression of p-ERK and p-p38MAPK proteins was significantly increased, after MDA-MB-231 cells were induced by shRANKL for 24 h. However, the increased effects induced by shRANKL were significantly attenuated by UO126 and SB202190 treatments. Conclusion ERK/p-38MAPK signal pathway may be involved in the migration and invasion of breast cancer MDA-MB-231 cells.

关 键 词：乳腺癌 胞外信号调节激酶 p-38丝裂原活化蛋白激酶 肿瘤侵袭 肿瘤转移 

分 类 号：R73-37[医药卫生—肿瘤]