Mechanism of sulforaphane in treatment of pancreatic cancer cell based on network pharmacology and in vitro experiments.

Sulforaphane (SFN), a bioactive compound derived from cruciferous vegetables, exhibits anti-cancer properties, though its role in pancreatic cancer is poorly understood. Network pharmacology and molecular docking (computer-simulated) identified the p53 pathway as a potential SFN target. In vitro experiments demonstrated that SFN suppressed PANC-1 cell proliferation and metastasis, induced G2/M arrest, and promoted apoptosis. Western blot analysis revealed SFN-mediated downregulation of cyclin B1 and CDK1 (linked to cycle arrest), upregulation of E-cadherin, and suppression of MMP-9 (impeding invasion). SFN also modulated apoptosis markers (Caspase-3/9 activation, Bax/Bcl-2 imbalance) and activated the p53 pathway (elevated p-p53, p53, p21, and GADD45A). These results underscore SFN's therapeutic potential against pancreatic cancer via p53 signaling.