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目的研究低剂量内皮-单核细胞激活多肽II(EMAP II)对U251胶质瘤细胞迁移和侵袭行为的影响及相关分子机制。方法 EMAP II(0.05n M)分别处理U251细胞不同时间后,采用Transwell小室实验及Matrigel Transwell小室实验检测U251细胞迁移和侵袭的变化,应用Western blot方法检测Fox O1和p-Fox O1的表达变化;转染Fox O1的沉默质粒(sh Fox O1)到U251细胞中,检测Fox O1敲减后EMAP II作用下U251细胞迁移和侵袭行为的改变。结果 EMAP II作用0.5 h和1 h时显著抑制U251细胞的迁移和侵袭行为;与EMAP II作用0 h组相比,Fox O1的表达在EMAP II作用0.5 h和1 h时显著升高,而p-Fox O1的表达显著下降;此外,sh Fox O1可减弱EMAP II对U251细胞迁移和侵袭行为的抑制作用。结论 EMAP II抑制U251细胞的迁移和侵袭,其机制可能与Fox O1的表达上调有关。
Objective To investigate the effect of low dose of endothelial cell-monocyte activating polypeptide II (EMAP II) on the migration and invasion of U251 glioma cells and the related molecular mechanisms. Methods The migration and invasion of U251 cells were detected by Transwell chamber assay and Matrigel Transwell chamber assay after treated with EMAP II (0.05nM) for different time. The expression of FoxO1 and p-FoxO1 was detected by Western blot. Transfect the FoxO1 silencing plasmid (sh Fox O1) into U251 cells and detect the migration and invasion of U251 cells induced by EMAP II knockdown by Fox O1. Results EMAP II significantly inhibited the migration and invasion of U251 cells at 0.5 h and 1 h. Compared with EMAP II group, the expression of Fox O1 increased significantly at 0.5 h and 1 h, while p FoxO1 expression decreased significantly; In addition, sh Fox O1 can attenuate EMAP II U251 cell migration and invasion inhibition. Conclusion EMAP II inhibits the migration and invasion of U251 cells, which may be related to the up-regulation of FoxO1 expression.