Huihua Wu*, Yu Xia**, Danling Jiang*, Xingqiu Guan*, Xi Li*, Ao Zou*, Tengfei Lu*, Junping Wang*, #


*Department of Gastroenterology, Peking University Shenzhen Hospital, Shenzhen, PR China - **Department of Oncology, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, PR China


Objective: To investigate the effect of Apatinib on MGC-803 cells in gastric cancer and the mechanism of possible signal pathway.

Methods: Human gastric cancer MGC-803 cells were selected to detect the effects of Apatinib on the toxicity, growth cycle, apoptosis, and VEGFR2-PLC-ERK1/2 pathway of human gastric cancer MGC-803 cells by using CCK-8 assay, propidium iodide staining, Annexin-V/PI double staining method, and Western blot assay, respectively.

Results: The CCK-8 assay showed that Apatinib can significantly inhibit the growth of MGC803 cells in human gastric cancer, and in a concentration-dependent manner. Propidium iodide staining showed that the observation group was obviously blocked in the G1 phase (P<.01). Annexin-V/PI double staining showed no statistically significant difference in early apoptosis rates between the observation group and the control group (P>.05). The Western blot assay showed that there was no significant change in the expression of ERK1/2, PLC, and other proteins after Apatinib treatment at different doses (0 μM, 10 μM, 20 μM, 40 μM, 80 μM) compared with a control group (P > .05). Moreover, the expression levels of p-ERK1/2 and p-PLC proteins decreased remarkably (P<.05).

Conclusion: Apatinib can block the growth cycle of gastric cancer MGC803 cells to inhibit cell proliferation. This may be achieved by inhibiting the phosphorylation of the VEGFR2-PLC-ERK1/2 signal pathway, leading to the obstruction of DNA synthesis in MGC803 cells. This result is not related to apoptosis.


Apatinib, gastric cancer MGC803 cells, VEGFR2-PLC-ERK1/2 signal pathway.