中文摘要：

目的 探讨敲低Abl相互作用蛋白1（Ablinteractor1，ABI．1）对胃癌NCI．N87细胞体外增殖和迁移能力的影响。方法利用脂质体和嘌呤霉素筛选稳定表达ABI．1短发夹RNA（shorthairpinRNA，ShRNA）的NCI—N87模型细胞，用实时定量RT-PCR和Westernblot鉴定ABI．1敲低的效果；用CCK-8试剂盒、细胞骨架染色和Transwell小室检测ABI-1敲低对细胞增殖、形态和骨架以及迁移的影响；用Westernblot检测磷酸化AKT蛋白的表达。结果成功获得表达ABI-1．ShRNA的NCI-N87细胞模型。CCK-8法检测显示NCI-N87-Vector和NCI-N87细胞在36h和48h的增殖率之间相比差异均无统计学意义（t=0．400、0．489，P〉0．05），而NCI．N87．ABI－1－ShRNA在36h和48h这2个时间点的增殖率均低于NCI－N87细胞（t=2．85、4．166，P〈0．05），ABI－1敲低抑制NCI．N87细胞的增殖。细胞骨架染色显示ABI-1敲低能够改变90％NCI－N87细胞的形态和骨架结构。Transwell研究显示NCI-N87、NCI－N87－Vector和NCI-N87-ABI-l—ShRNA的细胞迁移数分别是66±8、65±8和30±4，前两者相比差异无统计学意义（t=0．269，P〉0．05），敲低组与NCI．N87相比差异有统计学意义（t=9．550，P〈0．05），ABI－1敲低抑制NCI-N87细胞的迁移。WesternBlot显示ABI－1敲低抑制磷酸化AKT蛋白的表达。结论ABI-1敲低可能通过P13K／AKT通路抑制胃癌细胞NCI—N87的体外增殖和迁移。

英文摘要：

Objective To investigate the effects of ABI-1 gene knockdown upon the proliferation and migration of human gastric cancer cell NCI-N87 in vitro. Methods NCI-N87-ABI-1-ShRNA cell model was successfully constructed and validated by Real-time PCR and Western blot. The cellular morphous and skeleton, proliferative and migrative potents, and also AKT expression were compared between NCI-N87- ABI-1-ShRNA and its parents by immunofluorental staining, CCK-8 assay, transweU chamber and Western blotting. Results CCK-8 assay showed there was no significant difference in the proliferation rates at different time points between the NCI-N87-Vector and NCI-N87 cells while the proliferation rates at the time points of 36 and 48 hours of the NCI-N87-ABI-1-ShRNA were significantly lower than the NCI-N87 （t = 2. 85 and 4. 166 ,P 〈0. 05）. Transwell assay showed that migrated cell number were 66 ± 8, 65 ± 8 and 30 ± 4, respectively, and there was significant difference between the NCI-N87-ABI-1-ShRNA and NCI-N87 cells （t =9. 550,P 〈 O. 05）. Finally, ABI-1- knock-down altered the cellular morphous and skeleton of 90% NCI-N87 cells and inhibited p-AKT expression. Conclusion ABI-1 inhibits proliferation and migration of NCI-N87 cells in vitro probably by PI3K/AKT pathway.