Astragalus polysaccharide hinders cervical cancer immune escape by targeting NR3C2 and activating SLC40A1

Astragalus polysaccharides (APS) show promising effects in preventing tumor progression and immune escape. This study investigated the mechanism of APS in immune escape in cervical cancer (CC). The effects of different APS concentrations on the viability of CC cell lines (HeLa and SiHa) were determined. Immune evasion by CC cells was examined after APS treatment. An in vivo model was constructed by subcutaneous injection of U14 cells, and the effect of APS on immune evasion was investigated. APS downstream targets were screened using multiple databases, and the regulatory relationship between APS and NR3C2 was verified. Bioinformatics analysis was conducted to identify the downstream molecules of NR3C2, and the regulatory mechanism was validated. The effects of NR3C2 and SLC40A1 on immune escape were tested in vivo and in vitro. APS inhibited immune escape in CC and activated NR3C2 expression and CD8⁺ T cell function. NR3C2 knockdown reversed the inhibitory effects of APS on immune escape and malignant behaviors of CC cells. NR3C2 was enriched in the SLC40A1 promoter and promoted SLC40A1 expression. SLC40A1 upregulation enhanced the inhibitory effect of APS on immune escape in CC. APS inhibits immune escape of CC by targeting NR3C2 and activating SLC40A1.