Cuproptosis provides a new therapeutic strategy for cancer treatment and is thought to have broad clinical application prospects. Nevertheless, some oncological clinical trials have yet to demonstrate favorable outcomes, highlighting the need for further research into the molecular mechanisms underlying cuproptosis in tumors. Cuproptosis primarily hinges on the intracellular accumulation of copper, with lipid metabolism exerting a profound influence on its course. The interaction between copper metabolism and lipid metabolism is closely related to cuproptosis. Copper imbalance can affect mitochondrial respiration and lipid metabolism changes, while lipid accumulation can promote copper uptake and absorption, and inhibit cuproptosis induced by copper. Anomalies in lipid metabolism can disrupt copper homeostasis within cells, potentially triggering cuproptosis. The interaction between cuproptosis and lipid metabolism regulates the occurrence, development, metastasis, chemotherapy drug resistance, and tumor immunity of cancer. Cuproptosis is a promising new target for cancer treatment. However, the influence of lipid metabolism and other factors should be taken into consideration. This review provides a brief overview of the characteristics of the interaction between cuproptosis and lipid metabolism in cancer and analyses potential strategies of applying cuproptosis for cancer treatment.