抑制NSCLC细胞株H1299中EIF5A2表达对肿瘤生长及转移的影响

目的 研究真核翻译起始因子5A2(eukaryotic translation initiation factor 5A2, EIF5A2)在非小细胞肺癌(non-small cell lung cancer, NSCLC)细胞株H1299中的作用和潜在分子机制。方法 采用EIF5A2干扰RNA,敲除NSCLC细胞株H1299中的EIF5A2后,评估细胞的增殖能力、细胞凋亡率、细胞迁移和侵袭能力；采用Western印迹法检测NSCLC细胞株H1299敲除EIF5A2后,肿瘤相关蛋白和E-cadherin的表达情况。结果 EIF5A2的表达在NSCLS细胞株H1299中上调。而在体外实验中,EIF5A2的沉默可以抑制肿瘤细胞生长并诱导凋亡,降低细胞的迁移和侵袭能力,上调c-Myc、Bcl-2、Rac1表达,下调E-cadherin的表达。结论 EIF5A2可以促进NSCLC细胞株H1299的增殖和转移,可能成为NSCLS药物作用新靶点。
ObjectiveTo investigate the role of eukaryotic translation initiation factor 5A2 (EIF5A2) in non-small cell lung cancer (NSCLC) H1299 cell line. Methods EIF5A2 iRNA was transfected into NSCLC H1299 cells. After silencing of EIF5A2, proliferation, apoptosis, migration and invasion ability of H1299 cells were determined, the expression of tumor-related proteins and E-cadherin was detected with Western blotting. Results EIF5A2 expression was up-regulated in NSCLC H1299 cells. After silencing of EIF5A2, cell growth was reduced, cell apoptosis was increased, the migration and invasion ability was inhibited in H1299 cells; meanwhile the expression of c-Myc, Bcl-2, Rac1 was down-regulated and E-cadherin was up-regulation. Conclusion EIF5A2 may be associated with the malignancy of NSCLC H1299 cells, suggesting that it might be a potential therapeutic target for NSCLC