环巴胺对人食管癌EC109细胞转移的影响及作用机制  

Inhibitory effect of cyclopamine on metastatic ability of EC109 cells and its mechanism

作　　者：左小平[1] 秦治明[1] 王凯斌[1] 郑相如[1] 陈立前[1] 

机构地区：[1]重庆医科大学附属第一医院胸心外科,重庆400016

出　　处：《南方医科大学学报》2012年第12期1828-1832,共5页Journal of Southern Medical University

基　　金：重庆市卫生局重点课题基金(20121015)

摘　　要：目的探讨环巴胺特异性阻断人食管癌EC109细胞Hedgehog(Hh)信号通路后对其转移能力的影响及其可能的机制。方法环巴胺处理EC109细胞48 h后,采用Transwell小室、血管生成实验观察细胞的迁移、侵袭及血管形成等转移能力,RT-PCR检测Gli-1mRNA的表达,Western blot检测Gli-1、MMP-9、VEGF蛋白的表达。结果环巴胺阻断Hh信号通路能显著减弱EC109细胞迁移、侵袭及血管形成能力(P<0.05);Gli-1mRNA表达量降低,Gli-1、MMP-9、VEGF蛋白的表达量均降低,差异有统计学意义(P均<0.05)。结论环巴胺能显著抑制EC109细胞的转移能力,其可能机制与抑制Gli-1进而使下游MMP-9、VEGF表达下调有关。Objective To investigate the effect of cyclopamine on metastatic ability of human esophageal cancer EC109 cells and explore the possible mechanism. Methods Transwell chamber assay and angiogenesis assay were used to examine the metastatic ability, invasiveness and angiogenesis of EC109 cells treated with cyclopamine for 48 h. The expression of Gli-1 mRNA was detected using RT-PCR, and Western blotting was used to examine the protein expressions of Gli-1, matrix metalloproteainse-9 （MMP-9） and vascular endothelial growth factor （VEGF）. Results Inhibition of the hedgehog signaling pathway by cyclopamine suppressed the migration, invasion, and angiogenesis of EC109 cells. Cyclopamine treatment significantly lowered the expression of Gli-1 mRNA （P〈0.05） and the protein expressions of Gli-1, MMP-9 and VEGF （P〈0.05）. Conclusion Cyclopamine can significantly inhibit the metastatic capacity of EC109 cells possibly by down-regulating MMP-9 and VEGF expression as a result of Gli-1 inhibition.

关 键 词：HEDGEHOG通路 环巴胺 EC109细胞系 转移 

分 类 号：R735.1[医药卫生—肿瘤]