Research Progress on Copper Metabolism, Cuprotosis, and Their Regulatory Mechanism in Tumor Diagnosis and Treatment

A co-factor of multiple metalloenzymes that promote normal physiological functions, such as the immune system, neurological system, human hematological function, bone health, and antioxidant action, copper is one of the most important trace metals in the human body. The copper content in the human body maintains a relatively constant level; too much copper can cause Wilson's disease, and too little can cause Menkes disease. Copper is involved in the physiological functions of many body systems and has a very complex transport system with many transporters. In order to offer fresh concepts and a theoretical foundation for cancer treatment, this article will go into great detail about the distinct metabolic pathways of copper and the function of cell death, particularly the function of copper-controlled cell death, especially cuproptosis, in cancer detection and treatment. Cuproptosis, a copper-dependent cell death distinct from necrosis, apoptosis, and ferroptosis, is triggered by excessive intracellular copper binding to lipoylated tricarboxylic acid (TCA) cycle proteins, leading to abnormal protein aggregation and loss of iron-sulfur clusters in respiratory chain complexes. Future research may focus on optimizing the specificity of copper metabolism-related biomarkers (eg, CTR1, SOD1) for early tumor screening, developing targeted copper ionophores/chelators with low systemic toxicity, and exploring the crosstalk between copper metabolism and tumor immunity to establish multi-dimensional diagnosis and treatment strategies.