Apatinib suppresses the Proliferation and Apoptosis of Gastric Cancer Cells via the PI3K/Akt Signaling Pathway

• Published in: Journal of B.U.ON. : official journal of the Balkan Union of Oncology Vol. 24; no. 5; p. 1985
• Main Authors: Jia, Xiaoqiong, Wen, Zhenping, Sun, Qiuying, Zhao, Xiaohua, Yang, Hao, Shi, Xiaoyu, Xin, Tao
• Format: Journal Article
• Language: English
• Published: Greece 01.09.2019
• Subjects: Apoptosis - drug effects; Caspases - metabolism; Cell Line, Tumor; Cell Proliferation - drug effects; Humans; Phosphatidylinositol 3-Kinase - metabolism; Phosphorylation - drug effects; Proto-Oncogene Proteins c-akt - metabolism; Pyridines - pharmacology; Signal Transduction - drug effects; Stomach Neoplasms - drug therapy; Stomach Neoplasms - metabolism
• ISSN: 2241-6293

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. 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 are as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 was observed by 3-(4,5)-dimethylthiahiazo-(z-y1)-3,5-diphenytetrazoli- umromide (MTT) assay; (2) flow cytometry was adopted 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 (WB), 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. (1) MTT results showed that Apatinib could effectively inhibit the proliferation of HGC-27 cells in a dose-dependent manner. (2) Flow cytometry results manifested 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 pro-apoptotic 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. The experiment 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 on phosphorylation of the PI3K/Akt signaling pathway.