Targeting SRC to mediate solasonine’s anti-cancer activity in hepatocellular carcinoma and its potential for multi-cancer therapy

Introduction Cancer remains a leading cause of mortality worldwide, with persistent therapeutic gaps across its heterogeneous subtypes. Solasonine, a steroidal glycoalkaloid from Solanum species, exhibits broad anti-tumor activity, yet its pan-cancer mechanisms of action remain poorly defined. Methods A multi-tiered framework was employed: bibliometric analysis mapped the global research landscape; network pharmacology identified core solasonine-cancer target intersections, followed by GO and KEGG pathway enrichment and drug-target-pathway network construction; qRT-PCR, Western blotting, and CCK-8 assays in HCC cell lines experimentally validated the in silico-predicted hub target, SRC, and interrogated downstream signaling. Results Bibliometric analysis showed solasonine research concentrated primarily on breast cancer, bladder cancer, and HCC. Network pharmacology identified eight core targets—SRC, EGFR, AKT1, CDH1, TNF, BCL2, ESR1, and STAT3—with SRC as the central network hub. Experimental validation confirmed solasonine suppressed SRC at both transcriptional and translational levels, and SRC overexpression significantly rescued solasonine-induced proliferative inhibition in HCC cells. Discussion These integrated findings identify SRC as a critical mechanistic node mediating the pan-cancer anti-tumor effects of solasonine, particularly in HCC, and provide a rational foundation for its further development as a multi-target therapeutic agent.