c-Src在RANKL诱导的乳腺癌MDA-MB-231细胞迁移中的作用

摘要

目的 探讨非受体酪氨酸激酶c-Src在核因子-kB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-kB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 Trans well technique was used to assay the migration of breast cancer cells MDA-MB-231. The expression 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.