Cellular metabolism is essential for maintaining cell growth and self-renewal, providing energy, raw materials, and intermediates for biomolecule synthesis, and regulating enzyme activity to sustain normal cellular functions. Ferroptosis is a recently discovered form of iron-dependent programmed cell death, and its inhibition plays a crucial role in tumorigenesis and tumor progression. However, the role of cellular metabolism, particularly glucose and amino acid metabolism, in cancer ferroptosis is not well understood. This review discusses the involvement of glucose, lipid, amino acid, iron, and selenium metabolism in cancer cell ferroptosis, elucidating the impact of different metabolic pathways on this process. It also provides a detailed overview of agents used to induce cancer ferroptosis. The metabolism of tumor cells plays a crucial role in maintaining intracellular redox homeostasis, and disrupting normal metabolic processes in these cells renders them more susceptible to iron-induced cell death, resulting in enhanced tumor cell killing. The combination of ferroptosis inducers and cellular metabolism inhibitors may be a novel approach to future cancer therapy. Ferroptosis is a programmed cell death resulting from membrane damage caused by lipid peroxidation in an ion-dependent manner, and it is different from apoptosis, necrosis, pyroptosis, and autophagic death. Ferroptosis is closely linked to the development of diseases, and studies have shown that ferroptosis plays an important role in neurological diseases, ischemia-reperfusion injury, kidney injury, hematological diseases, and tumorigenesis. Increasing evidence has shown that ferroptosis exerts an important inhibitory effect on the progression of tumors. In most tumor cells, ferroptosis signaling is inhibited, suggesting that suppression of ferroptosis signaling may play a crucial role in tumorigenesis and that targeted induction of ferroptosis may lead to a significant breakthrough in cancer therapy. Therefore, understanding the regulation of iron-mediated cell death signaling in tumor cells is crucial for the accurate diagnosis and effective treatment of tumors. Cellular metabolism is the basis of normal physiological cellular functions. It contains the metabolism of biological macromolecules and other factors, such as trace elements (including iron and selenium). Biological macromolecule metabolism involves glucose, fatty acid, and amino acid metabolism, which generates ATP and provides the building blocks necessary for nucleic acid, lipid, and protein synthesis, thereby supporting cellular life processes. Trace element metabolism, such as iron and selenium metabolism, plays a crucial role in regulating the activity of various enzymes within cells and the essential cofactors needed for normal cellular growth. Simultaneously, the modulation of cellular signaling is influenced by alterations in cellular metabolism. In recent years, numerous studies have demonstrated the pivotal regulatory role of cell metabolism in tumor cell ferroptosis. In this review, we expound upon the roles of glucose metabolism, fatty acid metabolism, amino acid metabolism, iron metabolism and selenium metabolism in tumor ferCellular metabolism is essential for maintaining cell growth and self-renewal, providing energy, raw materials, and intermediates for biomolecule synthesis, and regulating enzyme activity to sustain normal cellular functions. Ferroptosis is a recently discovered form of iron-dependent programmed cell death, and its inhibition plays a crucial role in tumorigenesis and tumor progression. However, the role of cellular metabolism, particularly glucose and amino acid metabolism, in cancer ferroptosis is not well understood. This review discusses the involvement of glucose, lipid, amino acid, iron, and selenium metabolism in cancer cell ferroptosis, elucidating the impact of different metabolic pathways on this process. It also provides a detailed overview of agents used to induce cancer ferroptosis. The metabolism of tumor cells plays a crucial role in maintaining intracellular redox homeostasis, and disrupting normal metabolic processes in these cells renders them more susceptible to iron-induced cell death, resulting in enhanced tumor cell killing. The combination of ferroptosis inducers and cellular metabolism inhibitors may be a novel approach to future cancer therapy. Ferroptosis is a programmed cell death resulting from membrane damage caused by lipid peroxidation in an ion-dependent manner, and it is different from apoptosis, necrosis, pyroptosis, and autophagic death. Ferroptosis is closely linked to the development of diseases, and studies have shown that ferroptosis plays an important role in neurological diseases, ischemia-reperfusion injury, kidney injury, hematological diseases, and tumorigenesis. Increasing evidence has shown that ferroptosis exerts an important inhibitory effect on the progression of tumors. In most tumor cells, ferroptosis signaling is inhibited, suggesting that suppression of ferroptosis signaling may play a crucial role in tumorigenesis and that targeted induction of ferroptosis may lead to a significant breakthrough in cancer therapy. Therefore, understanding the regulation of iron-mediated cell death signaling in tumor cells is crucial for the accurate diagnosis and effective treatment of tumors. Cellular metabolism is the basis of normal physiological cellular functions. It contains the metabolism of biological macromolecules and other factors, such as trace elements (including iron and selenium). Biological macromolecule metabolism involves glucose, fatty acid, and amino acid metabolism, which generates ATP and provides the building blocks necessary for nucleic acid, lipid, and protein synthesis, thereby supporting cellular life processes. Trace element metabolism, such as iron and selenium metabolism, plays a crucial role in regulating the activity of various enzymes within cells and the essential cofactors needed for normal cellular growth. Simultaneously, the modulation of cellular signaling is influenced by alterations in cellular metabolism. In recent years, numerous studies have demonstrated the pivotal regulatory role of cell metabolism in tumor cell ferroptosis. In this review, we expound upon the roles of glucose metabolism, fatty acid metabolism, amino acid metabolism, iron metabolism and selenium metabolism in tumor fer