MEK/ERK信号通路在RANKL诱导的乳腺癌MCF-7细胞迁移中的作用及机制探讨

The Role of MEK/ERK pathway in RANKL-induced breast cancer cell MCF-7 migration

目的探讨细胞外调节蛋白激酶(ERK)信号通路在核因子-κB受体活化因子配体(RANKL)诱导的乳腺癌细胞MCF-7迁移中的作用。方法流式细胞术检测MCF-7细胞表面核因子-κB受体活化因子(RANK)蛋白的表达;Western blot检测RANKL刺激后磷酸化ERK(p-ERK)及ERK的表达;Transwell法测定RANKL刺激后细胞迁移能力的改变。结果 MCF-7细胞表面表达RANK蛋白,RANKL(2μg/mL)显著诱导MCF-7细胞迁移能力增强。RANKL刺激后MCF-7细胞p-ERK表达逐渐升高,MEK抑制剂PD98059显著抑制RANKL诱导的MCF-7细胞迁移。结论 ERK信号通路参与RANKL诱导的乳腺癌细胞MCF-7迁移。

Objective To explore the role of extracellular signal-regulated kinase in receptor activator for nuclear factor kappaB ligand（RANKL） induced breast cancer cells migration.Methods Receptor activator for nuclear factor kappaB（RANK） protein expression on the surface of breast cacner MCF-7 cell was detected by fluorescence-activated cell sorting（FACS）.Western blot assayed the expression of phospho-ERK and ERK.Transwell assayed the migration of MCF-7 cells.Results Fluorescence-activated cell sorting showed that RANK was expressed in human breast cancer cell line MCF-7,and RANKL significantly promoted the migration of MCF-7 cells.The expression of phospho-ERK increased from 5 to 30 minutes after RANKL stimulation.PD98059,the MEK inhibitor obviously blocked RANKL-induced MCF-7 cells migration.Conclusion ERK pathway was involved in RANKL induced breast cancer cell MCF-7 migration.