SRF/SLC31A1 signaling promotes cuproptosis induced by celastrol in NSCLC.

Faced with the highly malignant challenge of lung cancer, traditional chemotherapeutic agents, although predominantly inducing apoptosis, are severely limited in their therapeutic effect by the overexpression of anti-apoptotic proteins in lung cancer. Recently discovered copper-induced non-apoptotic cell death, known as cuproptosis, represents a novel mechanism for regulating cell death. Whether Celastrol (Cel), a potential anti-tumor drug, can counter non-small cell lung cancer (NSCLC) through inducing cuproptosis remains to be thoroughly investigated.