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Abstract To investigate the impact the signaling pathway of vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor 2 (VEGFR2) regulated by sevoflurane on the proliferation, apoptosis, and angiogenesis of the endometrial cancer cells. Methods: The endometrial cancer cells HEC-1A were divided into control group, sevoflurane group, si-NC group, si-VEGF group, sevoflurane+pc-NC group, and sevoflurane+pc-VEGF group. MTT and Edu methods were used to detect the proliferation of the endometrial cancer cells. Transwell test was used to detect the migration and invasion of the cells. Flow cytometry was used to detect the apoptosis rate of the cells. Matrigel gel three-dimensional culture was used to observe angiogenesis of the cells. The qRT-PCR was used to detect the expression levels of VEGF mRNA and VEGFR2 mRNA of the endometrial cancer cells in each group. Western blot was used to detect the expression levels of vascular endothelial growth factor A (VEGF-A), vascular endothelial cadherin (VE-cadherin), nuclear protein (Ki-67), cysteine protease-3 (Caspase-3), and VEGF/VEGFR2 signaling pathway related proteins of the endometrial cancer cells. Results: The HEC-1A cells in the control group had good lumen structure. Compared with those of the HEC-1A cells in the control group, the lumen structure of the HEC-1A cells in the sevoflurane group, in the si-VEGF group, and in the sevoflurane+pc-NC group had been disrupted significantly, the OD490 values in 24h and 48h, the cell proliferation rate, the numbers of cell migration and invasion, the expression of VEGF mRNA and VEGFR2 mRNA, and the expression levels of VEGF-A, VE cadherin, Ki-67, VEGF, and VEGFR2 proteins of the HEC-1A cells in the sevoflurane group, in the si-VEGF group, and in the sevoflurane+pc-NC group had decreased significantly, and the apoptosis rate and the expression of Caspase-3 protein of the HEC-1A cells in the sevoflurane group, in the si-VEGF group, and in the sevoflurane+pc-NC group had increased significantly (P＜0.05). There were no statistically significant differences in the detection indicators of the HEC-1A cells between the si-VEGF group and the sevoflurane group (P＞0.05). Compared with those of the HEC-1A cells in the sevoflurane+pc-NC group, the damage degree of the lumen structure of the HEC-1A cells had decreases significantly, the OD490 values in 24h and 48h, the proliferation rate, the numbers of migration and invasion, the expression levels of VEGF mRNA and VEGFR2 mRNA, and the expression levels of VEGF-A, VE cadherin, Ki-67, VEGF, and VEGFR2 proteins of the HEC-1A cells had increased significantly, the apoptosis rate and the expression of Caspase-3 protein had decreased significantly (all P＜0.05). Conclusion: Sevoflurane can inhibit the proliferation and angiogenesis of the endometrial cancer cells by blocking the VEGF/VEGFR2 signaling pathway, and can promote the apoptosis of the endometrial cancer cells.
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