Cancer cells undergo significant metabolic reprogramming to support rapid proliferation and survival in hostile environments. Key metabolic alterations, including glycolysis, oxidative phosphorylation (OXPHOS), and amino acid metabolism, allow cancer cells to meet high energy and biosynthetic demands. The Warburg effect highlights the dependence of cancer cells on glycolysis for rapid ATP production and biosynthetic intermediates, while mitochondrial flexibility enables shifts between glycolysis and OXPHOS under metabolic stress. Amino acids like glutamine and serine are crucial for cancer cell growth and survival. Therapeutic strategies targeting these altered pathways, such as glycolysis inhibitors, OXPHOS disruptors, and amino acid metabolism blockers, have shown promise in preclinical and clinical studies by disrupting tumor energy supply and biosynthesis. Combining metabolic inhibitors with chemotherapy, radiotherapy, and immunotherapy may enhance therapeutic efficacy, reduce resistance, and improve outcomes. However, challenges like drug delivery barriers, metabolic plasticity, and tumor heterogeneity complicate clinical translation. Personalized approaches, including metabolomic profiling, real-time imaging, and adaptive treatment strategies, offer the potential to tailor metabolic therapies to individual patients. Advances in drug delivery systems and technologies like CRISPR-Cas9 and AI-driven drug discovery are accelerating the development of precise metabolic therapies, offering promising avenues for improving cancer treatment outcomes.