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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BT474迁移中的作用。方法:流式细胞术及蛋白质印迹法检测BT474细胞表面RANK蛋白的表达;蛋白质印迹法检测RANKL刺激后细胞磷酸化ERK(p-ERK)及ERK的表达;Transwell法测定RANKL刺激后BT-474细胞迁移能力的改变。结果:BT-474细胞表面表达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,迁移增加率分别为(73.67±7.57)%和(9.67±3.06)%,P=0.001 5。BT-474细胞的P-ERK水平在RANKL刺激30min后明显升高,应用MEK/ERK通路抑制剂PD98059可显著抑制RANKL诱导的细胞迁移。RANKL迁移增加率为(72.50±6.61)%,RANKL+PD98059迁移增加率为(15.00±2.16)%,P=0.000 1。结论:ERK1/2信号通路参与RANKL诱导的乳腺癌BT-474细胞迁移。
AIM: To investigate the role of the extracellular regulated protein kinase (ERK) signaling pathway in the migration of BT474 cells induced by RANKL. Methods: The expression of RANK protein on BT474 cells was detected by flow cytometry and Western blotting. The expression of phosphorylated ERK (p-ERK) and ERK was detected by Western blotting. The expression of p-ERK and ERK was detected by Western blotting. Migration change. RESULTS: RANK protein was expressed on the surface of BT-474 cells and the migration ability of BT-474 cells was enhanced by RANKL. The use of RANKL as a decoy receptor could block RANKL-induced cell migration, the rate of increase was (73.67 ± 7.57)% and 9.67 ± 3.06)%, P = 0.001 5. The level of P-ERK in BT-474 cells was significantly increased after RANKL stimulation for 30min, and MEK / ERK pathway inhibitor PD98059 significantly inhibited RANKL-induced cell migration. The increase rate of RANKL migration was (72.50 ± 6.61)%, and the increase rate of RANKL + PD98059 migration was (15.00 ± 2.16)%, P = 0.000 1. Conclusion: The ERK1 / 2 signaling pathway is involved in RANKL-induced migration of breast cancer BT-474 cells.