Narrative review highlights lipid metabolism's role in gastric cancer progression, suggesting therapy targets for resistance.
Lipid metabolism plays a pivotal role in gastric cancer (GC) progression, characterized by complex metabolic reprogramming that supports tumor growth and survival. This narrative review comprehensively examines the dysregulation of lipid metabolism-associated genes, including fatty acid synthase (FASN), ATP-citrate lyase, acetyl-CoA carboxylases, FA binding proteins, sterol regulatory element-binding proteins, and other key enzymes. These genes facilitate critical oncogenic processes by enhancing FA synthesis, modifying cellular signaling, and supporting cancer cell proliferation, migration, and therapy resistance. Metabolic adaptations observed in GC include increased de novo lipogenesis, altered enzymatic activities, and modified protein lipidation, which contribute to tumor aggressiveness. The review highlights the potential of targeting these metabolic pathways as a therapeutic strategy, demonstrating how inhibiting specific enzymes like FASN, ATP-citrate lyase, and stearoyl-CoA desaturase 1 can induce apoptosis, disrupt cancer stem cell properties, and potentially overcome treatment resistance. By elucidating the intricate interactions between lipid metabolism genes and cancer progression, this review provides insights into novel diagnostic and therapeutic approaches for managing GC.
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Amir et al. (2025) studied this question.
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