ObjectiveTo explore the effects of apatinib on the proliferation, apoptosis and the VEGFR pathway of gastric cancer cells. MethodsHGC-27 and NCI-N87 cells belonged to gastric cancer cell lines were selected, and the effects of different concentrations of apatinib on the proliferation of HGC-27 and NCI-N87 cells were investigated by CCK-8 cell proliferation test and clone formation test. Flow cytometry was used to detect the effect of apatinib in different concentrations on the apoptosis of HGC-27 and NCI-N87 cells. Western blot was used to detect the effects of different concentrations of apatinib on the apoptosis-related proteins (Bcl-2, Bax, Caspase 3, Cleaved-Caspase 3) and vascular endothelial growth factor receptor 2 (VEGFR2) expression of HGC-27 and NCI-N87 cells. ResultsThe results of CCK-8 cell proliferation test and clone formation test showed that, with the increase of the apatinib concentrations, the survival rate of NCI-N87 and HGC-27 cells and the number of cell clones gradually decreased. The detective results of flow cytometry expressed that along with the increase of the concentrations of apatinib, the apoptosis rate of NCI-N87 and HGC-27 cells increased significantly. Western blot results revealed that as the concentrations of apatinib increased, the expression level of Bcl-2 decreased, whereas the expression levels of Bax and Cleaved-Caspase 3 increased, and the expression level of VEGFR2 decreased in both NCI-N87 and HGC-27 cells. ConclusionApatinib can inhibit the proliferation of gastric cancer cells and promote apoptosis, which may be related to its ability to regulate the expression levels of apoptosis-related proteins and VEGFR pathway-related proteins.

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