转化生长因子β1通过ERK/MAPK信号转导通路促进脑胶质瘤细胞侵袭  

Transforming growth factor β1 enhances the invasiveness of human glioma cell line via ERK/MAPK pathway

作　　者：刘丽华[1] 代勤[2] 闵志刚[2] 张明[2] 

机构地区：[1]西安交通大学医学院第一附属医院神经内科,陕西西安710061 [2]西安交通大学医学院第一附属医院影像中心,陕西西安710061

出　　处：《南方医科大学学报》2013年第12期1744-1747,共4页Journal of Southern Medical University

基　　金：国家自然科学基金(81171318)~~

摘　　要：目的探讨转化生长因子β1对脑胶质瘤细胞SF767细胞侵袭能力的影响以及可能的分子机制。方法转化生长因子β1分别干预脑胶质瘤细胞SF767细胞12、24、48 h,Western blotting检测EMT和ERK/MAPK通路相关蛋白表达情况,MTT法检测和对比干预前后细胞增殖情况,体外侵袭实验观察细胞侵袭能力改变。结果 Western blotting显示E-cadherin表达下调,而Vimentin和MMP-2表达上调。在ERK/MAPK信号转导通路中,ERK表达未见变化,但P-ERK表达上调,核转录因子Zeb-1表达增强。体外增殖实验显示干预后细胞倍增时间明显缩短;体外侵袭实验显示干预后穿膜细胞明显增多,统计学显示有显著性差异(P<0.05)。结论转化生长因子β1可能通过ERK/MAPK信号转导通路诱导EMT促进脑胶质瘤细胞SF767细胞侵袭。Objective To investigate the effect of transforming growth factorβ1 （TGF-β1） on the invasiveness of human glioma SF767 cell line in vitro and explore the possible molecular mechanism. Methods Human glioma SF767 cell line treated with TGF-β1 for 12, 24, or 48 h were examined for the expressions of epithelial-mesenchymal transition-and ERK/MAPK pathway-associated proteins using Western blotting. MTT assay and Transwell assay were employed to assess the changes in the cell proliferation and invasiveness after TGF-β1 treatment, respectively. Results Western blotting showed that TGF-β1 treatment up-regulated the expressions of vimentin, MMP-2, P-ERK, and Zeb-1 and down-regulated E-cadherin expression in SF767 cells. TGF-β1 treatment of the cells resulted in significantly shortened doubling time of cells and obviously increased cell invasiveness. Conclusions TGF-β1 induces epithelial-mesenchymal transition of SF767 cell line to increase its invasiveness possibly via ERK/MAPK pathway.

关 键 词：转化生长因子Β1 上皮间质转化 ERK MAPK信号转导通路 脑胶质瘤 E-CADHERIN 

分 类 号：R739.4[医药卫生—肿瘤]