首页> 中文期刊> 《山东医药》 >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

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

         

摘要

Objective To explore the role of extracellular signal-regulated kinase in receptor activator for nuclear fac tor kappaB ligand ( RANKL) induced breast cancer cells migration. Methods Receptor activator for nuclear factor kap paB (RANK) protein expression on the surface of breast cacner MCF-7 cell was detected by fluorescence-activated cell sor ting (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 mi gration. Conclusion ERK pathway was involved 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.

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