Objective To explore the mechanism of vasohibin 2 (VASH2) on angiogenesis of glioma by regulating the proliferation, migration and tube formation of glioma microvascular endothelial cells. Methods After cell model of human glioma microvascular endothelial cells (GECs) was obtained, VASH2 overexpression and silencing cell lines were established by stable transfection. In the follow-up experiment, they were divided into control group, VASH2 overexpression negative control empty plasmid[VASH2(+)NC] group, VASH2 overexpression [ VASH2(+) ]group, VASH2 expression silencing negative control empty plasmid [VASH2 (-) NC ]group and VASH2 expression silencing [VASH2(-)] group. Cell counting kit-8 (CCK-8) assay was used to detect cell proliferation, tube formation assay was employed to observe the changes of cell tube formation, and transwell assay was adopted to measure cell migration ability. GraphPad Prism v5.01 statistical software was used for data analysis. One-way ANOVA was employed for comparison between multiple groups and Newman-Keuls analysis was used for pairwise comparison between groups.Results When the expression of VASH2 was up-regulated in GECs, there was significant difference between VASH2(+) group and VASH2(+)NC group (P<0.05). The cell proliferation ability, migration ability and tube formation ability were significantly enhanced. It showed that VASH2 overexpression can promote the angiogenesis of glioma. When the expression of VASH2 was down-regulated, there was significant difference between VASH2(-) group and VASH2 (-) NC group (P<0.05). The proliferation ability, migration ability and tube formation ability of cells were significantly weakened, indicating that VASH2 silencing can inhibit the angiogenesis of glioma. Conclusion VASH2 plays an important role in the regulation of glioma angiogenesis. VASH2 may be considered as a potential target in the therapy for glioma in the future.