Deoxyelephantopin induces cell death in oral cancer cells via the downregulation of AKT1-mTOR-mediated mechanisms

DET effectively disrupts AKT1/mTOR signalling, inducing apoptosis and oxidative stress in OSCC cells. Its high biocompatibility (SWISS-ADME) and strong molecular interactions support its potential as a novel therapeutic agent for OSCC. This integrative approach provides valuable insights into DET's mechanism of action, paving the way for pre-clinical and clinical applications.