Fatty acid metabolism-related enzymes in colorectal cancer metastasis: from biological function to molecular mechanism

Abstract

Colorectal cancer (CRC) is a highly aggressive and life-threatening malignancy that metastasizes in ~50% of patients, posing significant challenges to patient survival and treatment. Fatty acid (FA) metabolism regulates proliferation, immune escape, metastasis, angiogenesis, and drug resistance in CRC. FA metabolism consists of three pathways: de novo synthesis, uptake, and FA oxidation (FAO). FA metabolism-related enzymes promote CRC metastasis by regulating reactive oxygen species (ROS), matrix metalloproteinases (MMPs), angiogenesis and epithelial-mesenchymal transformation (EMT). Mechanistically, the PI3K/AKT/mTOR pathway, wnt/β-catenin pathway, and non-coding RNA signaling pathway are regulated by crosstalk of enzymes related to FA metabolism. Given the important role of FA metabolism in CRC metastasis, targeting FA metabolism-related enzymes and their signaling pathways is a potential strategy to treat CRC metastasis.