Fig. 2

Overview of fatty acid metabolism in tumor cells. Tumor cells reprogram their lipid metabolism, impacting FA uptake (red- dotted line frame), de novo lipogenensis (DNL) (orange-dotted line frame), and activation (green- dotted line frame) of FAs and FAs oxidation (FAO) (blue-dotted line frame). The uptake of exogenous FAs in cancer cells mainly occurs through the process of fatty acid endocytosis, mediated by specialized transporters, including fatty acid translocase (FAT)/CD36, fatty acid transport protein family (FATPs) and plasma membrane fatty acid-binding proteins (FABPpm) [38]. DNL is a crucial component in cancer cell metabolism because of its importance in connecting glucose metabolism and lipid metabolism by catalyzing Acetyl-CoA, a product in glucose metabolism, to synthesis FAs [40, 41]. FAs in the cytoplasm are covalently modified under the catalysis of acyl-CoA synthetases (ACSs) to generate FA acyl-CoA esters that enter the bioactive pool to participate in the subsequent series of anabolism, catabolism, and oxidation. After activation in cytoplasm, FA acyl-CoA moves to the mitochondria to enter fatty acid β-oxidation (FAO), which is a multi-step reaction that involves various enzymes [60]