EFFECT OF OXYMATRINE ON BIOLOGICAL CHARACTERISTICS OF GASTRIC CANCER CELLS BY REGULATING PI3KAKT PATHWAY

Jinwei Cheng, Zhijin Yu, Cheng Luo, Yuanyuan Zhang, Huixin Chen^*

Department of Gastroenterology, Huizhou Central People’s Hospital, Huizhou 516001, Guangdong Province, China

Objective: To analyze the effect of oxymatrine (OMT) on the biological characteristics of gastric cancer cells by regulating the PI3KAkt pathway. 

Methods: The objective of the study is to analyze the effect of OMT on the biological characteristics of gastric cancer cells by regulating the PI3KAkt pathway. SGC-7901 gastric cancer cells were cultured and divided into a control group and an experimental group. The cells in the experimental group were divided into a low-dose group and a high-dose group, adding 1.0 and 3.0 g/L OMT, respectively. The control group was not treated with any drugs. An MTT assay was used to detect cell proliferation, flow cytometry was used to detect the apoptosis rate, and a western blot was used to detect cell proliferation and apoptosis-related proteins. In addition, enzyme-linked immunosorbent assay (ELISA) was used to detect VEGF protein expression, and a western blot was used to detect the PI3KAkt pathway-related protein. 

Results: The cell proliferation inhibition rate of the experimental group was significantly higher than that of the control group. With an increase of drug concentration and time, the cell proliferation inhibition rate gradually increased (P<0.05). The apoptosis rate of the experimental group was significantly higher than that of the control group, and the apoptosis rate of the high-dose group was significantly higher than that of the low-dose group (P<0.05). Ki67 and PCNA proteins in the experimental group were significantly lower than those in the control group, and caspase-9 protein was significantly higher than that in control group. In addition, Ki67 and PCNA proteins in the high-dose group were significantly lower than those in the low-dose group, and caspase-9 protein was significantly higher than seen in the low-dose group (P<0.05). VEGF protein in the experimental group was significantly lower than that in the control group, and the VEGF protein in the high-dose group was significantly lower than that in the low-dose group (P<0.05). The protein levels of PI3K and p-Akt in the experimental group were significantly lower than those in the control group, while those in the high-dose group were significantly lower than those in the low-dose group (P<0.05). 

Conclusion: OMT can inhibit the proliferation of gastric cancer cells, with the inhibition rate proportional to the action time and drug concentration. Moreover, OMT can induce apoptosis and inhibit the expression of tumor angiogenesis factors, which may be related to the regulation of PI3KAkt pathway by OMT.