PI3K/AKT信号通路在RANKL诱导的SGC-7901胃癌细胞迁移中的作用  

The role of PI3K/AKT pathway in RANKL-induced gastric cancer cell SGC-7901 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》2012年第8期52-54,共3页Shandong Medical Journal

基　　金：国家青年科学基金资助项目(30700807);辽宁省教育厅科技项目(2010225032)

摘　　要：目的文献报道RANKL/RANK/OPG途径与肿瘤细胞迁移及骨转移密切相关,但RANKL/RANK途径是否参与胃癌细胞迁移,尚无文献报道。本文拟检测RANK在胃癌细胞系SGC-7901细胞中的表达,并进一步探讨磷脂酰肌醇-3-激酶/丝苏氨酸蛋白激酶(PI3K/Akt)信号通路在RANKL诱导的胃癌细胞迁移中的作用。方法 West-ern blot检测SGC-7901细胞表面RANK蛋白的表达;RANKL刺激后磷酸化Akt(P-Akt)及Akt的表达;Transwell法测定RANKL及抑制剂刺激后细胞迁移能力的改变。结果 SGC7901细胞表达RANK蛋白。RANKL(1μg/mL)诱导SGC-7901细胞迁移能力增强,迁移增加率为57.2%±5.9%,RANKL抑制剂rOPG(5μg/mL)显著抑制RANKL诱导的细胞迁移(13.88%±3.57%,P<0.05)。RANKL刺激后30 min～3 h,SGC-7901细胞p-Akt表达升高,应用PI3K的抑制剂LY294002(50 mmol/L)显著抑制RANKL诱导的胃癌细胞SGC-7901的迁移(57.28%±5.91%vs23.18%±2.79%,P<0.05)。结论胃癌细胞系SGC-7901细胞表达受体RANK,PI3K/Akt信号通路参与RANKL诱导的SGC-7901细胞迁移。Objective To detect the expression of RANK in gastric cancer cell line SGC-7901 cell,and to explore the role of phosphoinositide 3-kinase/serine/threonine protein kinase（PI3K/Akt） pathway in RANKL-induced gastric cancer cell migration.Methods Cell-surface expression of RANK protein and the expression of phospho-Akt,Akt were detected by Western blot assay.Transwell assay was used to detect the migration of gastric cancer cells respectively.Results Western blot showed that RANK was expressed in human gastric cancer cell line SGC-7901,and RANKL increased the migration of gastric cancer cells significantly.rOPG,the specific inhibitor of sRANKL obviously blocked RANKL-induced gastric cancer cell migration.Akt was activated from 30 minutes to 3 hours after RANKL stimulated.LY294002,the PI3K inhibitor significantly inhibited RANKL-induced SGC-7901 cells migration.Conclusions This study provided for the first time that RANKL promoted RANK-expressing gastric cancer cell line SGC-7901 cell migration,and PI3K/Akt was involved in RANKL-induced gastric cancer cell migration.

关 键 词：AKT RANKL 胃肿瘤 迁移 

分 类 号：R733[医药卫生—肿瘤]