Aim To explore the effect of dasatinib on proliferation, migration, cell cycle and apoptosis of human umbilical vein endothelial cells cytologically and molecularly to offer help on clinical application of dasatinib. MethodsExperimental grouping:dasatinib group (dasatinib concentration was 50 nmol/L) and LY294002 group (PI3K inhibitor,concentration was 20 μmol/L), combined treatment group (dasatinib treatment concentration was 50 nmol/L, the concentration of LY294002 for 20 μmol/L) and mock group (DMSO was 0.1%). Cell viability was measured by CCK8. The migration ability of human umbilical vein endothelial cells was measured by scratch assay. Apoptosis and cell cycle were analyzed by flow cytometry. The expression and phosphorylation of Akt protein were determined by Western blot. Results The cell viability of human umbilical vein endothelial cells decreased gradually following the increasing concentration (1~400 nmol/L) and prolonged exposure to dasatinib (50 nmol/L, 24~96 h). Dasatinib and LY294002 (an inhibitor of PI3K), both inhibited cell viability of human umbilical vein endothelial cells. Dasatinib (50~100 nmol/L) weakened the migration capability of human umbilical vein endothelial cells. In addition, compared with control, dasatinib (50 nmol/L) induced apoptosis and cell cycle arrest (P＜0.05) of human umbilical vein endothelial cells. The phosphorylation of Akt was inhibited by dasatinib and LY294002, and LY294002 had more powerful inhibition of p-Akt than dasatinib. Conclusion Dasatinib could facilitate the injures of human umbilical vein endothelial cells via PI3K/Akt pathway, mainly to suppress the proliferation and migration of human umbilical vein endothelial cells, alter the cell morphology, blocked the G1-S transition and induced apoptosis.