<p>Copper-induced cell death, referred to as cuproptosis, introduces a new approach for cancer treatment by utilizing the toxic effects of copper. While copper is vital for enzymatic processes, it becomes harmful at excessive concentrations. Cuproptosis is characterized by mitochondrial impairment resulting from copper interacting with lipoylated components of the tricarboxylic acid (TCA) cycle, leading to proteotoxic stress and targeted cell death. This mechanism is distinct from traditional apoptosis and necrosis. Disruption of copper balance and associated genes, such as FDX1, LIAS, and DLAT, has been linked to various types of cancer. In this review, we outline the timeline of cuproptosis discovery and its comparison with other cell death mechanisms. In addition, we discuss copper homeostasis and copper metabolism in normal human physiology. We also reviewed how the disruption of copper balance can lead to cuproptosis and its involvement in tumorigenesis. Furthermore, we provided an overview of the various genes associated with cuproptosis and their roles in cancer. Given the numerous targets identified, we also provide a thorough overview of the drugs linked to cuproptosis and discuss their clinical relevance and prospects. This review indicates that targeting cuproptosis may serve as a novel therapeutic approach for cancer treatment.</p> Graphical abstract <p></p>