c-Src参与RANKL诱导的乳腺癌BT-474细胞迁移的机制研究

目的：核因子-κB受体活化因子配体（RANKL）/核因子κB受体活化因子（RANK）通路在肿瘤骨定向性迁移中发挥重要的作用,但具体信号传导机制尚不清楚。本文探讨非受体酪氨酸激酶c-Src在RANKL诱导的乳腺癌BT474细胞迁移中的作用。方法：Western blot检测BT-474细胞表面受体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。采用SPSS 16.0统计学软件分析实验数据。结果：BT-474细胞表达RANK蛋白,RANKL诱导BT-474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BT-474细胞p-Src表达升高,应用c-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BT-474细胞迁移。

c-Src involved in RANKL-induced breast cancer cell BT-474 migration

Objective： It was recently reported that RANKL（also referred to as OPGL,TRANCE or ODF） plays an important role in RANK-expressing tumor cells migration and the bone-specific metastasis of cancer cells.But the signal pathway of RANKL/RANK in tumor cells migration is unclear.The present study was aimed to explore the role of c-Src in regulation of BT-474 breast cancer cells migration by RANKL.Methods： Transwell was used to assay the migration of breast cancer cells BT-474.Western blotting was used to assay the expression of RANK,phospho-Src,c-Src and actin.Results： RANK was expressed in human breast cancer cell line BT-474,and RANKL significantly increased the migration of BT-474 cells.The decoy receptor OPG significantly blocked the increased migration.c-Src was activated after RANKL stimulated,PP2,the c-Src inhibitor obviously inhibited RANKL-induced BT-474 cells migration.Conclusion： c-Src was involved in RANKL-induced breast cancer BT-474 cells migration.