Cancer cells reprogram their metabolism to meet the energy, biosynthetic, and redox demands of malignancy, a hallmark of cancer. This review outlines key principles of cancer metabolism, emphasizing how metabolic reprogramming supports tumorigenesis and metastasis. Metabolic reprogramming involves altered bioenergetics, biosynthesis, and redox balance, which are critical for cell survival and proliferation. These changes are driven by oncogenes like MYC and the PI3K-AKT-mTOR pathway, which promote anabolic processes. Tumor cells also adapt to hypoxia by increasing glycolysis and utilizing alternative metabolic pathways. Oncometabolites, such as D2HG, succinate, and fumarate, are metabolites that accumulate in tumors and contribute to cancer progression through nonmetabolic effects. Understanding these metabolic changes is essential for developing targeted therapies. Metabolic therapies, such as inhibiting glycolysis or targeting specific metabolic enzymes, have shown promise in preclinical models. However, challenges remain in translating these findings to clinical settings, as many metabolic pathways are essential for normal cells. Targeting metabolic pathways in cancer cells requires careful consideration of their physiological roles and potential toxicity. Emerging strategies include targeting multiple metabolic pathways simultaneously or combining metabolic therapies with other treatments. Key metabolic targets include enzymes involved in glycolysis, one-carbon metabolism, mitochondrial function, and redox balance. Inhibiting these pathways can disrupt cancer cell growth and survival, offering new therapeutic opportunities. The development of effective metabolic therapies will depend on understanding the context-specific roles of metabolic pathways in tumor progression and metastasis.Cancer cells reprogram their metabolism to meet the energy, biosynthetic, and redox demands of malignancy, a hallmark of cancer. This review outlines key principles of cancer metabolism, emphasizing how metabolic reprogramming supports tumorigenesis and metastasis. Metabolic reprogramming involves altered bioenergetics, biosynthesis, and redox balance, which are critical for cell survival and proliferation. These changes are driven by oncogenes like MYC and the PI3K-AKT-mTOR pathway, which promote anabolic processes. Tumor cells also adapt to hypoxia by increasing glycolysis and utilizing alternative metabolic pathways. Oncometabolites, such as D2HG, succinate, and fumarate, are metabolites that accumulate in tumors and contribute to cancer progression through nonmetabolic effects. Understanding these metabolic changes is essential for developing targeted therapies. Metabolic therapies, such as inhibiting glycolysis or targeting specific metabolic enzymes, have shown promise in preclinical models. However, challenges remain in translating these findings to clinical settings, as many metabolic pathways are essential for normal cells. Targeting metabolic pathways in cancer cells requires careful consideration of their physiological roles and potential toxicity. Emerging strategies include targeting multiple metabolic pathways simultaneously or combining metabolic therapies with other treatments. Key metabolic targets include enzymes involved in glycolysis, one-carbon metabolism, mitochondrial function, and redox balance. Inhibiting these pathways can disrupt cancer cell growth and survival, offering new therapeutic opportunities. The development of effective metabolic therapies will depend on understanding the context-specific roles of metabolic pathways in tumor progression and metastasis.