摘要目的 探讨巨噬细胞移动抑制因子(MIF)对胶质瘤细胞株U87MG、U251生物学功能的影响及可能的作用机制.方法 运用小于扰RNA(siRNA)技术靶向沉默U87MG细胞株中MIF基因的表达,经蛋白免疫印迹(Western blot)法检测沉默效果;对微弱表达MIF蛋白的U251细胞株,则外源性添加不同浓度重组人MIF(rhMIF).采用划痕实验观察细胞的迁移、流式细胞术检测细胞凋亡率,并经Western blot法检测U87MG、U251细胞内相关蛋白水平的变化.结果 经siRNA靶向沉默MIF基因表达后,U87MG细胞的迁移、抗凋亡能力明显下降,细胞内p-AKT、抗凋亡蛋白bcl-2表达水平下降,而凋亡蛋白bax表达升高;微弱表达MIF蛋白的U251细胞随着rhMIF处理浓度的增加,其细胞内MIF蛋白、p-AKT及bcl-2表达水平逐渐升高,凋亡蛋白bax水平则随之下降.结论 MIF促进胶质瘤细胞的迁移,抑制其凋亡,影响胶质瘤细胞生物学功能,可能是通过活化PI3K/AKT信号通路实现的.

abstractsObjective To investigate the effect of macrophage migration inhibitory factor (MIF) on the biology of glioma U87MG and U251 cells.Methods Silencing MIF gene expression in U87MG cells by RNA interference was monitored by Western blot.MIF low expressing U251 cells were treated at different concentrations of recombinant human MIF (rhMIF) and scratching test and flow cytometry were used to detect cell migration and apoptosis.The protein expression of bcl-2,bax,AKT,p-AKT was detected by Western blot.Results The ability of migration and anti-apoptosis of U87MG cells silenced by siRNA decreased significantly,and the expression levels of p-AKT and anti-apoptotic protein bcl-2 also decreased;in contrast,the expression level of apoptosis protein bax increased.With increase of rhMIF treatment concentration,the expression levels of MIF protein,p-AKT and bcl-2 in U251 cells were gradually enhanced,whereas the level of apoptosis protein bax was inhibited.Conclusion MIF promotes cell migration and inhibits apoptosis of both U87MG and U251 cells,likely through the regulation of PI3K/AKT signaling pathway.