【摘要】 探讨e IF4E在CXCL12诱导胃癌细胞形态学改变和迁移中的作用和机制.在胃癌细胞株(SGC7901,MGC803)上给予CXCL12处理,显微镜下观察细胞形态的改变;通过transwell实验检测CXCL12对胃癌细胞迁移能力的影响;在SGC7901上给予CXCL12处理,用Western blot检测e IF4E磷酸化和总蛋白水平的变化;用脂质体转染e IF4E的小干扰RNA,检测e IF4E对胃癌细胞形态学和迁移的影响;以及用qRT-PCR检测与肿瘤侵袭转移密切相关的因子MMP9的mRNA水平的表达.结果显示,给予CXCL12处理,胃癌细胞形态由上皮表型向长梭形的间叶样表型转变,细胞的迁移能力提高.在相同浓度的CXCL12处理情况下,转染e IF4E siRNA抑制e IF4E的表达,可抑制CXCL12诱导的细胞的形态学改变和迁移能力.另外,CXCL12引起与肿瘤转移密切相关因子MMP9的mRNA水平的表达升高,而用siRNA抑制e IF4E的表达,可下调MMP9的mRNA表达水平.结论:CXCL12激活了e IF4E,阻抑e IF4E的表达抑制CXCL12诱导的形态学改变和细胞迁移,其作用机制可能与上调MMP9的表达有关.更多还原

【Abstract】 To study of eIF4E in CXCL12 induced morphological changes and migration mechanism in gastric cancer cells.In gastric cancer cell lines( SGC7901,MGC803),cell morphological changes with CXCL12 treatment were observed under microscopy. The effect of CXCL12 on gastric cancer cell migration was determined by transwell assay. Western blot anlaysis was used to detect the eIF4 E phosphorylation and total protein levels in SGC7901 treated with CXCL12. MMP9 mRNA expression was determined by qRT-PCR assay. Results show that,CXCL12 induced gastric cancer cells from epithelial morphology to mesenchymal morphology as well as increased migration. Morphological changes and migratory capacity induced by CXCL12 were inhibited by e IF4 E siRNA transfection in SGC7901 cells. In addition,CXCL12 induced upregulation of MMP9 mRNA level. Conclusion: eIF4E is involved in CXCL12 induced the morphological changes and cell migration of gastric cancer cells possibility through upregulation of MMP9.更多还原