Targeting ATP7A-Dependent Copper Metabolic Homeostasis Induces Cuproptosis and Suppresses the Progression of Mutant KRAS-Driven Lung Cancer.

Despite progress in tumor-targeted therapy, oncogenic KRAS remains a major challenge in treating lung adenocarcinoma (LUAD). In clinical practice, KRASG12C inhibitors have limited response rates and are associated with acquired drug resistance. Cuproptosis is a recently identified form of copper (Cu)-mediated cell death, and previous studies have revealed that Cu metabolism plays an important role in the development of KRAS-driven tumors.