Fig. 1

Lipid metabolic reprogramming in cancer. Tumor cells enhance lipid metabolism by increasing exogenous lipid uptake and lipid synthesis, leading to increased intracellular lipid content. Upregulation of lipid transport proteins such as CD36, FATPs, FABPs, and LDLR increases lipid uptake. These upregulations increase intracellular SUFA, PUFA, and cholesterol levels. Meanwhile, endogenous lipid synthesis originates from citrate in the TCA cycle, as well as intracellular glutamine, lactate and acetate, leading to the synthesis of SFA and cholesterol. The process is catalyzed by key enzymes such as FASN and SCD. FAs in tumor cells are catalyzed by ACSL to form acyl-CoA, which is involved in the subsequent synthesis of intracellular phospholipids with bioactive lipids and FAO. Acyl-CoA facilitates the translocation of enzymes into mitochondria through CPT1, the key enzyme of FAO, participating in the production of acetyl-CoA, providing energy for the biological behavior of tumor cells. Excess lipids in tumor cells are stored in LD as CE and TAG. This storage significantly prevents LPO and attenuates its risk of mediating tumor cell death