Effects of radix actinidiae chinensis extracts on the proliferation and apoptosis of breast cancer cells by regulating the VEGF/PI3K/AKT signaling pathway / 中国医师杂志

ABSTRACT

Objective:To investigate the effects of radix actinidiae chinensis extracts on the proliferation and apoptosis of breast cancer cells by regulating the vascular endothelial growth factor (VEGF)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway.Methods:Human breast cancer cell line MCF7 was cultured in vitro and divided into control group, low-dose group, medium dose group and high-dose group. The low-dose, medium dose and high-dose groups were added with DMEM culture medium diluted with 1, 10 and 100 μg/ml radix actinidiae chinensis extracts respectively. The control group was added with equal dose DMEM culture medium for 48 hours. The proliferation rate (detected by methyl thiazolyl tetrazolium method), apoptosis rate (detected by flow cytometry) and the protein expression of PI3K, VEGF and phosphorylation-AKT(p-AKT) in each group were compared (detected by Western blot). Results:Compared with the control group, the proliferation rate and PI3K, VEGF, p-AKT protein expression of MCF7 cells in low dose group were significantly decreased ( P<0.05), and the apoptosis rate of MCF7 cells in low dose group was significantly increased ( P<0.05); compared with low dose group, the proliferation rate and PI3K, VEGF, p-AKT protein expression of MCF7 cells in medium dose group were significantly decreased ( P<0.05), and the apoptosis rate of MCF7 cells in medium dose group was significantly increased ( P<0.05). Compared with the middle dose group, the proliferation rate of MCF7 cells and the expression of PI3K, VEGF and p-AKT protein in the high dose group were significantly decreased ( P<0.05), and the apoptosis rate of MCF7 cells in the high dose group was significantly increased ( P<0.05). Conclusions:Radix actinidiae chinensis extracts may inhibit the proliferation and promote the apoptosis of breast cancer cells by inhibiting the VEGF/PI3K/AKT signaling pathway.