Cellular copper transport (CCT)

Cellular copper transport refers to the complex network of proteins responsible for maintaining copper homeostasis within the cell, including uptake via Solute Carrier Family 31 Member 1 (CTR1), intracellular distribution by chaperones like ATOX1 and CCS, and efflux via ATPases such as ATP7A and ATP7B (Source: UniProt, PubMed: 25407722). Copper is an essential cofactor for enzymes involved in respiration, antioxidant defense, and neurotransmitter synthesis, but its levels must be strictly regulated to prevent oxidative stress and proteotoxicity (Source: NIH, StatPearls). In oncology, cellular copper transport is targeted because rapidly proliferating cancer cells often exhibit an increased demand for copper to support angiogenesis and metabolic reprogramming (Source: PubMed: 30104618). Therapeutic strategies include the use of chelators to sequester copper or ionophores to induce copper-dependent cell death, known as cuproptosis (Source: Science, 2022). Dysregulation of this system is also the primary cause of genetic disorders such as Wilson disease and Menkes disease, as well as a contributing factor in neurodegenerative conditions like Alzheimer's and Parkinson's diseases (Source: PubMed: 29107491).

Other names

Copper homeostasisCopper transport systemCopper traffickingCopper metabolism

Copper chelation, copper ionophore-mediated transport, inhibition of copper uptake transporters (CTR1), and modulation of copper-transporting ATPases (ATP7A/B).