Fatty acid-binding proteins in cancers

作者：Long Wu, Guangfei Ou, Wei Zhang, Huaxing Ma, Xiaoyun Li, Yun-Huan Zhen, Huan Wu, Kun Cao, Hai-Yang Li · 发表于：International Journal of Surgery · 年份：2025 · DOI：10.1097/js9.0000000000003049 · 被引用次数：13 · 研究领域：Peroxisome Proliferator-Activated Receptors、Cancer, Lipids, and Metabolism、Inflammatory mediators and NSAID effects

Fatty acid-binding proteins (FABPs) are intracellular lipid chaperones with molecular weights of approximately 14-15 kDa. By binding and transporting fatty acids and lipid-related molecules, FABPs precisely regulate metabolic pathways, signal transduction, and gene expression, playing a central role in cancer initiation and progression. The 11 identified subtypes (FABP1-FABP12; FABP11 is identical to FABP3) exhibit tissue-specific expression and influence tumor progression through metabolic reprogramming, immune microenvironment modulation, and therapy resistance. Metabolically, FABPs enhance fatty acid uptake, β-oxidation, and synthesis, meeting the high proliferative demands of tumors. In immune regulation, FABP4 + macrophages secrete IL-6 to suppress T cell activity, while FABP6 downregulates MHC-I molecule expression to reduce CD8 + T cell infiltration, fostering an immunosuppressive microenvironment. Regarding therapy resistance, FABP4 enhances mitochondrial β-oxidation to reduce apoptosis in ovarian cancer, and FABP5 promotes chemoresistance in HCC via the HIF-1α pathway. Functional heterogeneity exists among subtypes: FABP7 drives glioblastoma stem cell migration via RXRα signaling, while FABP5 exhibits context-dependent roles, promoting HCC progression but suppressing colorectal cancer (CRC) through mTOR-mediated autophagy. Clinically, FABPs serve as diagnostic biomarkers and therapeutic targets. However, challenges such as insufficient target specificity, cross-cance...