Published online Aug 15, 2025. doi: 10.4251/wjgo.v17.i8.106842
Revised: April 12, 2025
Accepted: June 24, 2025
Published online: August 15, 2025
Processing time: 158 Days and 22.5 Hours
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.
Core Tip: Dysregulation of lipid metabolism plays a crucial role in gastric cancer (GC) progression by supporting tumor growth, migration, and therapy resistance. This review explores the oncogenic pathways involving key lipid metabolism-associated genes, including fatty acid synthase, ATP-citrate lyase, acetyl-CoA carboxylases, fatty acid binding proteins, and sterol regulatory element-binding proteins, highlighting their role in metabolic reprogramming. Targeting these pathways offers promising therapeutic strategies, as inhibiting lipid biosynthesis enzymes can induce apoptosis and disrupt cancer stem cell properties. Understanding the intricate link between lipid metabolism and GC may pave the way for novel diagnostic and therapeutic advancements.
