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tid Target Cancers General Effect on Target
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Beta-oxidation serves as a major pathway for breaking down fatty acids into acetyl-CoA, which then enters the tricarboxylic acid (TCA) cycle to generate ATP.

– In tumors with limited glucose availability or under metabolic stress, enhanced fatty acid oxidation can serve as an alternative energy source, supporting cell survival and proliferation.
– Beta-oxidation contributes to the removal of excess fatty acids and provides substrates for oxidative phosphorylation, thereby influencing the balance between energy production and biosynthetic needs.
– Tumor environments are often hypoxic and nutrient-deprived. Enhanced beta-oxidation can allow cancer cells to adapt by optimizing energy yield from available substrates.

– Upregulated beta-oxidation or reliance on fatty acid metabolism in certain tumors has been correlated with increased aggressiveness, metastasis, and a poor overall prognosis.




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