c-Src在RANKL诱导的乳腺癌MDA-MB-231细胞迁移中的作用  

Role of c-Src in RANKL-induced breast cancer cell MDA-MB-231 migration

作　　者：张凌云[1] 曲秀娟[1] 刘云鹏[1] 侯科佐[1] 

机构地区：[1]中国医科大学附属第一医院,沈阳110001

出　　处：《山东医药》2011年第44期4-6,118,共4页Shandong Medical Journal

基　　金：国家青年科学基金资助项目(30700807);辽宁省教育厅重点实验室项目(2008S246)

摘　　要：目的探讨非受体酪氨酸激酶c-Src在核因子-κB受体活化因子配体(RANKL)诱导的乳腺癌MDA-MB-231细胞迁移中的作用。方法流式细胞仪检测MDA-MB-231细胞表面受体核因子-κB受体活化因子(RANK)蛋白的表达及RANKL刺激后细胞p-Src及c-Src的表达;Transwell法测定细胞迁移能力。结果 MDA-MB-231细胞表达RANK蛋白,RANKL诱导MDA-MB-231细胞迁移能力增强。应用RANKL的圈套受体OPG可阻断RANKL诱导的细胞迁移。RANKL刺激后MDA-MB-231细胞p-Src表达升高,应用Src激酶抑制剂PP2可显著抑制RANKL诱导的细胞迁移。结论 c-Src信号通路参与RANKL诱导的乳腺癌MDA-MB-231细胞迁移。Objective To explore the role of c-Src in regulation of MDA-MB-231 breast cancer cells migration by RANKL. Methods Transwell technique was used to assay the migration of breast cancer cells MDA-MB-231. The expres- sion of RANK, phospho-Src, c-Src and actin were measured by Western blot method. Results RANK was expressed in human breast cancer cell line MDA-MB-231, and RANKL increased significantly the migration of MDA-MB-231 cells. The decoy receptor OPG significantly blocked the increased migration, c-Src was activated after RANKL stimulated, the c-Src inhibitor PP2 inhibited obviously RANKL-induced MDA-MB-231 cells migration. Conclusion c-Src was involved in RANKL-induced breast cancer MDA-MB-231 cell migration.

关 键 词：C-SRC 核因子-ΚB受体活化因子配体 乳腺肿瘤 迁移 

分 类 号：R737.9[医药卫生—肿瘤]