Cancer cells have distinct metabolic characteristics compared to normal cells, including increased aerobic glycolysis, fatty acid synthesis, and glutamine metabolism. These metabolic changes are linked to therapeutic resistance in cancer treatment. Targeting metabolic enzymes such as glucose transporters, hexokinase, pyruvate kinase M2, lactate dehydrogenase A, pyruvate dehydrogenase kinase, fatty acid synthase, and glutaminase can enhance the efficacy of cancer therapies and overcome resistance to chemotherapy or radiotherapy. Recent studies show that dysregulated metabolism contributes to drug resistance, and targeting these metabolic pathways may improve cancer treatment outcomes. Inhibiting metabolic enzymes can increase the effect of anticancer treatments or reduce resistance. For example, 2-deoxyglucose (2-DG) inhibits glycolysis, leading to cell death and increased sensitivity to chemotherapy. Similarly, inhibitors of fatty acid synthase (FASN) and glutaminolysis can enhance the effectiveness of chemotherapeutic agents. Targeting PDK, which regulates glycolysis, can also improve chemotherapy outcomes. Overall, targeting cancer metabolism represents a promising strategy to overcome drug resistance and improve cancer therapy.Cancer cells have distinct metabolic characteristics compared to normal cells, including increased aerobic glycolysis, fatty acid synthesis, and glutamine metabolism. These metabolic changes are linked to therapeutic resistance in cancer treatment. Targeting metabolic enzymes such as glucose transporters, hexokinase, pyruvate kinase M2, lactate dehydrogenase A, pyruvate dehydrogenase kinase, fatty acid synthase, and glutaminase can enhance the efficacy of cancer therapies and overcome resistance to chemotherapy or radiotherapy. Recent studies show that dysregulated metabolism contributes to drug resistance, and targeting these metabolic pathways may improve cancer treatment outcomes. Inhibiting metabolic enzymes can increase the effect of anticancer treatments or reduce resistance. For example, 2-deoxyglucose (2-DG) inhibits glycolysis, leading to cell death and increased sensitivity to chemotherapy. Similarly, inhibitors of fatty acid synthase (FASN) and glutaminolysis can enhance the effectiveness of chemotherapeutic agents. Targeting PDK, which regulates glycolysis, can also improve chemotherapy outcomes. Overall, targeting cancer metabolism represents a promising strategy to overcome drug resistance and improve cancer therapy.