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Mitochondrial dysfunction and the Warburg effect, characterized by aerobic glycolysis, are hallmarks of cancer metabolism, facilitating tumor progression and resistance to therapies. These metabolic shifts allow cancer cells to prioritize glycolysis over oxidative phosphorylation, contributing to rapid proliferation, immune evasion, and metastasis. This review explores the intricate regulation of the Warburg effect by enzymes, transcription factors, and non-coding RNAs. Key players, such as hexokinase, pyruvate kinase M2, and glucose transporters, are discussed as central drivers of glycolysis. This review highlights therapeutic strategies targeting these pathways, including small-molecule inhibitors, combination therapies, and traditional medicines. Advanced diagnostic tools, such as FDG-PET imaging and metabolic profiling, are evaluated for their potential to personalize cancer treatment. The role of synthetic lethality, immunotherapy, and novel drug combinations in addressing metabolic vulnerabilities is also examined. Furthermore, the review underscores the impact of metabolic reprogramming on the tumor microenvironment and its implications for immune modulation. Targeting the Warburg effect presents a promising avenue for overcoming drug resistance and enhancing cancer therapy. This review provides a comprehensive framework for integrating metabolic reprogramming into advanced therapeutic and diagnostic strategies, paving the way for personalized cancer treatment approaches.
