Abstract
Copper plays an essential role in numerous biological functions, requiring tight regulation to prevent toxicity and health complications. Cuproptosis is a recently discovered form of regulated cell death that occurs due to intracellular copper accumulation, with a unique mechanism distinct from other known cell death pathways. It is initiated when copper binds to lipoylated enzymes within the tricarboxylic acid (TCA) cycle, leading to enzyme aggregation, proteotoxic stress, and, ultimately, cell death. Since its identification, cuproptosis has drawn significant attention for its potential application in cancer therapy. Copper-based treatments have shown promise in suppressing tumor growth and may offer therapeutic strategies for tumors resistant to conventional chemotherapy. This article explores the underlying mechanisms of cuproptosis and the involvement of copper in various malignancies, aiming to advance targeted cancer therapies and inspire the development of novel anticancer agents that harness this pathway. Finally, important concepts of cuproptosis and issues to focus on in future studies are discussed.
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