<p>Ferroptosis and cuproptosis are two recently discovered forms of programmed cell death. Both forms of cell death are regulated by distinct yet interconnected pathways, and their roles in tumor progression and therapy response have gained much concern and are highly anticipated. Both involve alterations in cellular metabolism. Oxidative stress plays a crucial part in both processes. Ferroptosis mainly involves the peroxidation of cell membrane lipid components, while cuproptosis is more related to mitochondrial dysfunction and the stability of iron sulfur cluster proteins. Moreover, ferroptosis is usually related to iron and antioxidant capacity, while cuproptosis focuses more on the imbalance of copper homeostasis and its impact on organelles. The increase in reactive oxygen species can trigger DNA damage and other cellular stresses that impact tumor development and response to treatment. In ferroptosis, iron catalyzes the Fenton reaction, generating hydroxyl radicals that cause oxidative damage. Copper metabolism also intersects with iron metabolism. For example, copper chaperones such as copper chaperone for superoxide dismutase regulate intracellular copper levels and indirectly affect iron handling. Crosstalk between ferroptosis and cuproptosis involves diverse signaling pathways. In this review, we recapitulate the way these two sorts of programmed cell death interact, providing insights into mechanisms of therapeutic resistance. Targeting both pathways simultaneously or sequentially may well surmount resistance and boost treatment efficacy. In summary, the shared mechanisms and interplay between ferroptosis and cuproptosis offer exciting opportunities for enhancing our knowledge of tumor biology and improving cancer treatment paradigms. Continued research in this area promises to uncover new targets and strategies for treatment of cancer.</p>