Exploring the Role and Targets of Spatholobus suberectus Dunn in Cervical Cancer Therapy Via an Integrated Strategy of Network Pharmacology and in Vitro Experiments

Objective This study aimed to clarify the inhibitory effects of Spatholobus suberectus Dunn (SSD) on cervical cancer (CC) cells using network pharmacology. Methods We explored SSD’s mechanism and targets in CC therapy and identified potential therapeutic targets through comprehensive analysis. Active components of SSD were identified via the TCMSP database, and disease-related targets were sourced from TTD, GeneCards, OMIM, and PharmGKB. A Venn diagram identified intersecting targets, and the STRING database facilitated a protein-protein interaction network. Cytoscape visualized the active C-T-D network. GO and KEGG enrichment analyses were performed using R software. Molecular docking was verified with AutoDock and PyMOL, while the CCK-8 assay assessed SSD’s inhibitory effects on Caski cell proliferation at 24, 48, and 72 hours. The scratch assay evaluated SSD’s impact on cell migration, and RTCA tracked its effects on proliferation and migration over 72 hours. Flow cytometry examined apoptosis and cell cycle distribution post-SSD treatment. Protein expression levels of P27, P21, P53, and those in the PI3K/Akt and Jak2/Stat3 pathways were measured using the JESS automated Western blot system. Results Screening identified 24 active components from SSD. Analysis revealed 32,330 CC targets, with 119 overlapping drug-disease targets identified using Jvenn. KEGG pathway enrichment showed SSD significantly affects PI3K/Akt and P53 pathways. Molecular docking indicated strong binding of SSD’s active ingredients to key CC targets. CCK-8, scratch assays, and RTCA demonstrated SSD’s inhibitory effects on Caski cell proliferation and migration. Flow cytometry showed SSD induces apoptosis and cell cycle arrest in Caski cells. Jess assay results suggested SSD may inhibit CC progression by modulating pathways like P27, P21, P53, PI3K/Akt, and Jak2/Stat3. Conclusion SSD has a significant inhibitory effect on CC cells, though the mechanisms require further exploration.