Apatinib suppresses the proliferation and apoptosis of gastric cancer cells via the PI3K/Akt signaling pathway

Purpose: To observe the mechanism of the effects of Apatinib on the proliferation and apoptosis of human gastric cancer (HGC-27) cells via the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway through in vitro cytology experiments. Methods: The human gastric cancer HGC-27 cell line was taken as the research object, and LY294002, an inhibitor of the PI3K/Akt signaling pathway, as the positive control. The experimental methods were as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 were observed by MTT assay; (2) flow cytometry was performed to detect the apoptosis of cells after they were treated with drugs and the positive control; (3) different effects of varying concentrations of Apatinib on apoptosis-related genes and proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase) 9, were detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting, and the effects of different concentrations of Apatinib on the protein expressions of PI3K, phosphorylated (p)-PI3K, Akt and p-Akt were detected by Western blotting. Results: (1) MTT results showed that Apatinib could effectively inhibit the proliferation of HGC-27 cells in a dose-dependent manner. (2) Flow cytometry results showed that Apatinib could induce the apoptosis of HGC-27 cells. (3) The results of qRT-PCR and Western blotting demonstrated that Apatinib was capable of inducing the expression of the proa-poptotic genes, Bax and Caspase 9, and inhibit the expression of the anti-apoptotic gene Bcl-2. The final results of Western blotting confirmed that Apatinib could decrease the protein expression levels of p-PI3K and p-Akt, thus inhibiting the phosphorylation of the PI3K/Akt pathway. Conclusions: This study proves that Apatinib can effectively suppress the proliferation and induce the apoptosis of human gastric cancer HGC-27 cells, the mechanism of which is related to the inhibition of phosphorylation of the PI3K/Akt signaling pathway.