中文摘要：

目的：研究趋化因子受体CXCR4活化对胶质瘤干细胞（glioma stem cells,GSCs）迁移能力的影响,并探索其下游相关信号通路。方法：采用逐渐添加神经干细胞培养液的方法从人胶质细胞瘤U87细胞株中获得GSCs,利用Transwell小室法评估CXCR4活化对GSCs迁移能力的影响,并进一步应用Western印迹法观察CXCR4下游信号通路的激活情况。结果：CXCR4的配体CXCL12以浓度依赖的方式促进GSCs迁移,同时伴有Akt磷酸化增加;CXCR4特异性拮抗剂AMD3100能够抑制此效应。PI3K/Akt通路抑制剂LY294002可通过抑制Akt磷酸化而抑制CXCL12诱导的GSCs迁移。结论：CXCR4活化后激活其下游的PI3K/Akt信号通路,进而促进GSCs迁移,这可能是GSCs高侵袭特性的机制之一。

英文摘要：

Objective：To investigate the effect of CXCR4 activation on the migrating capacity of glioma stem cells （GSCs） and identify the corresponding downstream signal pathway responsible for the effect. Methods：GSCs were obtained by gradually adding neural stem cell culture medium. The migrating capacity of GSCs was measured using Transwell chamber assays.Western blotting was used to detect the activation of downstream signaling cascade.Results：CXCR4 ligand CXCL12 promoted GSCs migration and Akt phosphorylation in a concentration-dependent manner. AMD3100, a CXCR4 specific antagonist, significantly suppressed CXCL12-induced GSCs migration and Akt phosphorylation. LY294002, a PI3K/Akt pathway inhibitor, could inhibit CXCL12-induced GSCs migration via blocking the phosphorylation of Akt. Conclusion：CXCR4 activation can promote GSCs migration through activating the PI3K/Akt signaling pathway, which may be one of the mechanisms responsible for the high invasive capacity of GSCs.