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

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.