HMGA2在胃癌细胞SGC-7901上皮间质转化中的作用

目的 探讨TGF-β1调控人胃癌细胞SGC-7901由上皮向间质细胞转化过程中,HMGA2的表达及其作用。方法 用TGF-β1处理人胃癌细胞SGC-7901(0,3,6,24,48,72h),在显微镜下观察SGC-7901细胞形态的变化,蛋白质印记法检测HMGA2、E-cadherin和Vimentin蛋白的表达,Transwell小室实验检测细胞侵袭能力。结果 (1)随着TGF-β1作用时间的延长,SGC-7901细胞逐渐变长,变大,细胞融合;(2)在TGF-β1作用下,SGC-7901均不同程度地表达HMGA2、E-cadherin和Vimentin。HMGA2蛋白从0h开始表达,到6h表达最强,24h以后表达稍有下降。E-cad蛋白从0h开始表达,到3h表达最高,随后开始降低。Vimentin蛋白48h表达最高,72h有降低的趋势;(3)Transwell小室实验显示SGC-7901在TGF-β1处理后,3h时细胞穿膜最多,从6h起穿过的细胞开始降低,到72h最低。结论 在TGF-β1诱导人胃癌细胞SGC-7901细胞上皮间质转化的过程中,HMGA2蛋白起到重要作用,HMGA2可作为Snail的启动子,结合Smads,促进上皮间质转化HMGA2还可能通过调控Wnt/β-Catenin信号通路对肿瘤细胞的生长和凋亡发挥作用。

HMGA2 in the role of gastric cancer SGC-7901 epithelial-mesenchymal transition

Objective To investigate the role of HMGA2 expression and epithelial to mesenchymal cell transformation in the regulation of TGF-β1 in human gastric cancer cells.Methods Human gastric cancer cell SGC-7901 was treated by TGF-β1 at different time points(0,3,6,24,48,72h).We observed the changes in cell morphology of SGC-7901 through the microscope;HMGA2 assay,E-cadherin,Vimentin protein expression were performed by Western blot;cell invasion capability was analyzed by transwell chamber assay.Results (1)With the prolonged duration of action of TGF-β1,SGC-7901 changes in cell morphology,cells gradually became longer and larger.(2)In the role of TGF-β1,gastric cancer cells SGC-7901 are varying degrees of HMGA2 expression and E-cadherin、Vimentin.HMGA2 protein begun to express from 0h to 6hrs.and HMGA2 protein became the strongest at 6hrs and decreased slightly from 24hrs.E-cad protein expression at 0h begun at 3hrs highest expression,and the reduction started from 3hrs.Vimentin protein was the highest at 48hrs then gradually decreased.Conclusion In the TGF-β1 induced the process of epithelial to mesenchymal cell transformation in gastric cancer cells SGC-7901,HMGA2 protein play an important role.HMGA2 can be used as snail promoter,combined with Smads,promotes the process of epithelial-mesenchymal transformation.HMGA2 may also be regulated by Wnt / β-Catenin signaling pathway on growth and apoptosis of tumor cells.