eIF5A-2在非小细胞肺癌上皮间质化过程中的作用机制  

The role of eIFSA-2 in regulating epithelial-mesenchymal transition in non-small cell lung cancer

作　　者：邵国丰[1] 徐国栋[1] 史信宝[1] 孙东波[1] 周青云[1] 郑大为[1] 石活顺[1] 李旎[1] 

机构地区：[1]宁波市医疗中心宁波大学附属李惠利医院外科,315041

出　　处：《中华胸心血管外科杂志》2013年第9期528-531,共4页Chinese Journal of Thoracic and Cardiovascular Surgery

摘　　要：目的探讨真核细胞翻译起始因子5A-2（eIF5A-2）的表达在非小细胞肺癌（NSCLC）上皮间质化（EMT）过程中的作用及其机制。方法通过Westrn—blotting和免疫荧光检测细胞表型变化，利用siRNA转染下调eIF5A-2表达后再以Western—blotting和免疫荧光检测细胞表型的改变。用TGF-β1刺激诱导NSCLC细胞系NCI－H358和HCC827发生EMT后并利用Western—blotting检测eIF5A-2的表达。结果NCI—H358和HCC827细胞系低表达eIF5A-2，为上皮表型，而NCI—H1299细胞高表达eIF5A-2，为问质表型。eIF5A-2siRNA干扰后可以改变NCI—H1299细胞的间质表型。NCI—H358和HCC827细胞经TGF-β1诱导后可发生EMT变化，而eIF5A-2siRNA干扰后则可防止这种变化的发生。结论在不同的NSCLC细胞系中，间质表型细胞较上皮表型者高表达eIF5A-2。TGF-β1可诱导上皮表型细胞发生EMT，而干扰eIF5A-2则可阻止EMT的发生。Objective To investigate the effect and mechanism of elFSA-2 in regulating epithelial-mesenchymal transition（EMT） in non-small cell lung cancer （NSCLC）. Methods Western-blotting and immunofluorescence have been used to tested phenotype of different NSCLC cell lines. After interfering with elFSA-2 siRNA, we used western-blotting and immunoflu-orescence to test phenotype changes. TGF-I31 was used to induce NCI-H358 and HCC827 cells underwent EMT changes. Resuits NCI-H358 and HCC827 expressed low levels of eIFSA-2 and belonged to epithelial phenotype; while NCI-H1299 expressed high level of eIF5A-2 and belonged to mesenehymal phenotype. After down-regulating eIFSA-2 level by interfering with eIF5A-2 siRNA, NCI-HI299 changed to epithelial phenotype. NCI-H358 and HCC827 changed to mesenchymal phenotypes after stimulating with TGF-131 and eIFSA-2 siRNA could prevent this transition. Conclusion Mesenchymal phenotype NSCLC cells express high level of elFSA-2. TGF-ISI could induce epithelial phenotype NSCLC cells undergo EMT changes and interfering eIF5 A-2 could prevent this transition.

关 键 词：癌 非小细胞肺 上皮细胞 基因表达 分子作用机制 eIF5A-2 转化生 长因子β1 

分 类 号：R734.2[医药卫生—肿瘤]