Abstract

Bladder cancer cell viability and migration were assessed using CCK-8 and wound healing assays following SANC treatment. Molecular targets and pathways were predicted through network pharmacology and proteomic analysis. Reactive oxygen species (ROS) and glutathione (GSH) levels were measured to evaluate redox balance. The interaction between SANC and EGFR was validated via molecular docking and surface plasmon resonance (SPR). Protein expression was analyzed using Western blotting and immunofluorescence, and a xenograft mouse model was employed to assess in vivo anti-tumor efficacy. SANC significantly inhibited bladder cancer cell proliferation, colony formation, and migration. Mechanistically, it bound to EGFR and downregulated the PI3K/AKT/FOXO3a signaling pathway, leading to cell cycle arrest and apoptosis. SANC also increased Reactive Oxygen Species (ROS) levels and depleted Glutathione (GSH), contributing to redox imbalance and further suppression of EGFR activity. In vivo, SANC markedly reduced tumor growth without evident toxicity. SANC significantly inhibited bladder cancer cell proliferation, colony formation, and migration. Mechanistically, it bound to EGFR and downregulated the PI3K/AKT/FOXO3a signaling pathway, leading to cell cycle arrest and apoptosis. SANC also increased ROS levels and depleted GSH, contributing to redox imbalance and further suppression of EGFR activity. In vivo, SANC markedly reduced tumor growth without evident toxicity. SANC exerts potent anti-tumor effects against bladder cancer by directly targeting EGFR, inhibiting the PI3K/AKT/FOXO3a signaling axis, and disrupting redox homeostasis. These findings support the therapeutic potential of SANC as a novel EGFR-targeted agent for bladder cancer treatment.