Unravelling the Mechanism of Compound Kushen Injection in Treating Cervical Cancer Through Ferroptosis Regulation: An Integrated Network Pharmacology and Molecular Docking Study

ABSTRACT

This study employed network pharmacology and molecular docking techniques to investigate the potential mechanisms of Compound Ku Shen Injection in the treatment of cervical cancer (CC), focussing on ferroptosis. Active compounds and corresponding targets of CKI, as well as CC‐related targets, were identified from relevant databases. Intersecting targets between CKI and CC were used to construct a protein–protein interaction (PPI) network, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Core compounds and targets were further validated by molecular docking experiments. A total of 58 active compounds and 801 overlapping targets were identified in this study. Key active compounds included matrine, quercetin, diosgenin, luteolin, sophoramine, sophocarpine, formononetin, and kushenol J_qt2. Major target genes involved were IL6, PPARG, HIF1A, TP53, STAT3, EGFR, JUN, MTOR, RELA, and SRC. KEGG highlighted C‐type lectin receptor, AGE‐RAGE, HIF‐1, ErbB, and IL‐17 pathways in regulating ferroptosis. Molecular docking confirmed strong binding of compounds to TP53, HIF1A, PPARG, and IL6. Bioinformatics showed downregulation of JUN, PPARG, and RELA in CC patients, whereas TP53 and IL6 were upregulated. The Kaplan‐Meier curve suggested that high expressions of JUN and IL6 may serve as prognostic risk markers for CC. These findings suggest that CKI may exert potential anti‐CC effects via multi‐component, multi‐target, and multi‐pathway mechanisms, possibly involving ferroptosis‐related regulatory processes. This study provides a preliminary computational reference for future mechanistic and experimental investigations of CKI in cervical cancer.