南方医科大学学报

南方医科大学学报 ›› 2013, Vol. 33 ›› Issue (12): 1744-.

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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

刘丽华，代勤，闵志刚，张明   

  • 出版日期:2013-12-20 发布日期:2013-12-20

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

  • Online:2013-12-20 Published:2013-12-20

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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。

Abstract: Objective To investigate the effect of transforming growth factor β1 (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.