Sodium Cantharidate Suppresses Tongue Cancer Via Pi3k/Akt Pathway

This study aims to clarify the molecular mechanism of sodium cantharidate (SCA) against tongue squamous cell carcinoma (TSCC) through network pharmacology and experimental validation. Previous studies have indicated the potential of SCA in anti-cancer therapy, yet its role in TSCC remains unclear. Using TCMSP, PubChem, and Swiss Target Prediction databases, 68 overlapping targets of SCA against TSCC were identified. KEGG pathway analysis highlighted the PI3K/AKT signaling pathway as a key mediator. SCC-25 cells were treated with SCA (5–30 μmol/L) for 48 h. Cell viability was evaluated by CCK8 assay, colony formation by crystal violet staining, and apoptosis by flow cytometry. Western blotting was used to detect protein expression of PI3K/AKT pathway components and apoptosis-related markers. Data were analyzed using one-way ANOVA with GraphPad Prism 9.5.1(P<0.05 considered significant). SCA dose-dependently inhibited SCC-25 cell viability (P<0.01), suppressed colony formation and migration, and induced apoptosis (P<0.05). Mechanistically, SCA downregulated p-PI3K/PI3K, p-AKT/AKT, PCNA, and Bcl-2, while upregulating Bax. Co-treatment with the PI3K agonist 740Y-P partially reversed these effects. SCA exerts anti-TSCC effects by inhibiting the PI3K/AKT pathway, suggesting its potential as a novel therapeutic agent for TSCC. These findings provide preclinical evidence for SCA-based targeted therapy.