Cuproptosis is a novel form of copper-induced cell death distinct from traditional cell death mechanisms. It involves the interaction of copper with lipoylated tricarboxylic acid cycle (TCA) enzymes, leading to protein aggregation and cell death. Recent studies have linked cuproptosis to cancer development, highlighting its role in tumor progression, including cell proliferation, metastasis, and chemotherapy resistance. Copper metabolism and homeostasis are critical for cellular function, and dysregulation can contribute to cancer. Copper is absorbed in the gastrointestinal tract, transported via chaperones, and regulated by transporters like ATP7A and ATP7B. Copper is involved in various cellular processes, including antioxidant defense, mitochondrial function, and signaling pathways. Dysregulation of copper homeostasis can lead to oxidative stress, mitochondrial dysfunction, and cancer progression. Copper is also involved in key signaling pathways such as the PI3K-AKT, MAPK, and Notch pathways, which are crucial for cancer cell survival and growth. Cuproptosis is distinct from other forms of cell death, such as apoptosis, necrosis, and ferroptosis, and is characterized by mitochondrial dysfunction and lipid peroxidation. Copper ionophores like DSF and ES have been shown to induce cuproptosis, which can be combined with small molecule drugs for targeted cancer therapy. The interplay between cuproptosis and ferroptosis is complex, with both pathways contributing to cancer progression and treatment resistance. Understanding the molecular mechanisms of cuproptosis and its relationship with other cell death pathways is essential for developing novel therapeutic strategies in cancer treatment.Cuproptosis is a novel form of copper-induced cell death distinct from traditional cell death mechanisms. It involves the interaction of copper with lipoylated tricarboxylic acid cycle (TCA) enzymes, leading to protein aggregation and cell death. Recent studies have linked cuproptosis to cancer development, highlighting its role in tumor progression, including cell proliferation, metastasis, and chemotherapy resistance. Copper metabolism and homeostasis are critical for cellular function, and dysregulation can contribute to cancer. Copper is absorbed in the gastrointestinal tract, transported via chaperones, and regulated by transporters like ATP7A and ATP7B. Copper is involved in various cellular processes, including antioxidant defense, mitochondrial function, and signaling pathways. Dysregulation of copper homeostasis can lead to oxidative stress, mitochondrial dysfunction, and cancer progression. Copper is also involved in key signaling pathways such as the PI3K-AKT, MAPK, and Notch pathways, which are crucial for cancer cell survival and growth. Cuproptosis is distinct from other forms of cell death, such as apoptosis, necrosis, and ferroptosis, and is characterized by mitochondrial dysfunction and lipid peroxidation. Copper ionophores like DSF and ES have been shown to induce cuproptosis, which can be combined with small molecule drugs for targeted cancer therapy. The interplay between cuproptosis and ferroptosis is complex, with both pathways contributing to cancer progression and treatment resistance. Understanding the molecular mechanisms of cuproptosis and its relationship with other cell death pathways is essential for developing novel therapeutic strategies in cancer treatment.