EMAP-Ⅱ上调miR-429表达抑制人U87胶质瘤细胞的增殖、迁移和侵袭能力

Endothelial-monocyte-activating polypeptide Ⅱ inhibits proliferation, migration and invasion of U87 glioma cells by up-regulating the expression of miR-429

目的探讨内皮-单核细胞激活多肽-Ⅱ(EMAP-Ⅱ)对人U87胶质瘤细胞增殖、迁移和侵袭的影响以及可能的机制。方法培养人U87胶质瘤细胞,给予EMAP-Ⅱ处理不同时间后,采用CCK-8检测细胞活力的变化;应用real-time PCR方法检测mi R-429在人U87胶质瘤细胞中的表达变化;利用Lipofect AMINETM2000将antimi R-429及其阴性对照转染至人U87胶质瘤细胞,再给予EMAP-Ⅱ,分别应用CCK-8法和Transwell小室法检测人胶质瘤U87细胞的增殖、迁移及侵袭能力。结果与对照组相比,EMAP-Ⅱ显著抑制了人U87胶质瘤细胞的活力,上调mi R-429在人U87胶质瘤细胞的表达水平,上述变化在EMAP-Ⅱ作用0.5 h时效果最显著;与EMAP-II作用0.5 h组相比,转染anti-mi R-429后,EMAP-Ⅱ的作用被阻断,人胶质瘤U87细胞的细胞活力,以及迁移和侵袭能力基本恢复。结论 mi R-429参与了EMAP-Ⅱ抑制人U87胶质瘤细胞的增殖,迁移和侵袭的调控。

Objective To study the effects and potential mechanism of proliferation, migration and invasion of human glioma U87 cells regulated by endothelial-monocyte-activating polypeptide Ⅱ（EMAP-Ⅱ）. Methods Human U87 glioma cells were treated with EMAP-Ⅱ for different times, CCK-8 was used to detect the change of cell viability in U87 cells. Real-time PCR was used to detect the expression of mi R-429 in glioma U87 cells. Lipofect AMINETM2000 was used to transfect anti-mi R-429 and its negative control into human U87 glioma cells, and then treated with EMAP-Ⅱ, CCK-8 assay and Transwell chamber assay were applied to measure the proliferation, migration and invasion of human U87 glioma cells. Results Compared with control group, EMAP-Ⅱ inhibited the viability of U87 cells and improved the expression of mi R-429 in U87 cells obviously, these effects were most significant at the 0.5h after EMAP-Ⅱ treatment. In contrast to EMAP-Ⅱ 0.5h group, the effort of EMAP-Ⅱ was blocked by transfecting anti-mi R-429, the abilities of proliferation, migration and invasion of human glioma U87 cells were recovered. Conclusion mi R-429 was involved in the inhibition of EMAP-Ⅱon the proliferation, migration and invasion of U87 glioma cells.