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Effect of ginsenoside Rg3 on immune escape of breast cancer cells via regulating pentose phosphate pathway mediated by PI3K/AKT/mTOR signaling pathway
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Abstract:
[Abstract] Objective: To investigate the effect of ginsenoside Rg3 (GRG3) on the immune escape of breast cancer cells by regulating pentose phosphate pathway (PPP) mediated by PI3K/AKT/mTOR signaling pathway. Methods: MCF7 cells were routinely cultured and divided into five groups: control group, GRG3 low-dose (GRG3-L) group, GRG3 high-dose (GRG3-H) group, GRG3-H + 740Y-P (PI3K activator) group, and Ly294002 (PI3K inhibitor) group. Colony formation assay, flow cytometry, DCFH-DA fluorescent probe assay, and WB were used to evaluate cell proliferation, apoptosis, ROS levels, and the expression of proteins related to the PPP and the PI3K/Akt/mTOR signaling pathway in each group, respectively. The cytotoxic effect of NK-92MI cells against MCF7 cells was measured using the CCK-8 assay. ELISA was employed to detect the levels of CXCL-2, CXCL-8, G6PD, and NADPH in MCF7 cells, as well as the levels of TNF-α and IFN-γ in the culture supernatant of co-cultured cells. Results: GRG3 significantly suppressed the clonogenic ability of MCF7 cells (all P < 0.05), promoted apoptosis of MCF7 cells (all P < 0.05), and reduced the levels of CXCL-2, CXCL-8, G6PD, NADPH, and ROS in MCF7 cells (all P < 0.05). Additionally, GRG3 inhibited the PPP and PI3K/Akt/mTOR signaling pathways (all P < 0.05), promoted the secretion of TNF-α and IFN- γ by NK-92MI cells (all P < 0.05), and enhanced the cytotoxicity of NK-92MI cells against MCF7 cells (all P < 0.05). These effects were partially reversed by 740Y-P (P < 0.05). Conclusion: GRG3 inhibits the biological behavior and immune escape of breast cancer MCF7 cells by suppressing the PI3K/AKT/ mTOR pathway-mediated PPP.
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