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 explore the effect and mechanism of low-dose endothelial-monocyte activating polypeptide II (EMAP 11) on migration and invasion of U251 glioma cells. Methods The aheration of migration and invasion ability of U251 glioma cells after EMAP II treatment for different times was observed by Transwell assay and Matrigel Transwell assay. The expression of FoxO1 and p-FoxO1 proteins was detected by Western blot after EAMP II treatment. Moreover, we observed the alteration of migration and invasion ability by EMAP II treatment a/one or combination with FoxO1 knockdown through transfection with FoxO1 silence plasmids(shFoxO1). Resdts The inhibitory effect on migration and invasion of U251 glioma cells was detected after EMAP II treatment for 0.5 h and 1 h. The expression level of FoxO1 was significandy increased after EMAP II treatment for 0.5 h and 1 h, but decreased for p-FoxOlexpression. Furthermore, shFoxO1 markedly attenuated the inhibition effect on migration and invasion of U251 glioma cells by EMAP 11 treatment. The inhibitory effect on migration and invasion of U251 glioma cells was detected after EMAP 11 treatment for 0.5 h and 1 h. The expression level of FoxO1 was significantly increased after EMAP II treatment for 0.5 h and 1 h, but decreased for p-FoxO1 expression. Furthermore, shFoxO1 markedly attenuated the inhibition effect on migration and invasion of U251 glioma cells by EMAP II treatment, Condusion The inhibitory effect of lowdose EMAP II on migration and invasion of U251 glioma cells might be related to the up-regulation of FoxO1 expression.