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Over the past few years, de novo lipogenesis has taken central stage in the field of cancer metabolism (1). Large amount of lipids is needed for synthesis of membranes, signaling molecules, lipoproteins, etc. to support rapidly growing tumor cells (2-4). Reports have shown that neoplastic tissues show aberrant activation of de novo lipogenesis and that inhibition of different enzymes within the fatty acid biosynthesis pathway can block cancer cell growth (2, 5-9). Meanwhile, the importance of fatty acid oxidation (FAO) in cancer metabolism is being increasingly recognized. FAO is the catabolic process by which lipids are utilized to produce energy. Recent studies implicated that the key regulatory enzymes in FAO such as carnitine palmitoyltransferase 1 (CPT1) and peroxisomal acyl-coenzyme A oxidase 1 (ACOX1) regulate cancer development (10, 11). The underlying mechanisms for the regulation of de novo lipogenesis and FAO in cancers are, however, still incompletely understood. Thus, it would be of a high scientific and clinical interest to elucidate the lipid metabolism in cancer. Multiple independent laboratories discovered that CD147, a transmembrane glycoprotein, is highly expressed in hepatocellular carcinoma (HCC) cells and is strongly associated with tumor progression (12, 13). Licartin, an 131Iodin-labeled antibody fragment targeting the HCCassociated antigen HAb18G/CD147, has been approved by the Chinese Food and Drug Administration (FDA) and enters into clinical use for HCC treatment (14-16). To date, studies have shown that CD147 contributes to the metabolism of cancer cells via glycolysis (17-19). However, a paper recently published in the Journal of Hepatology by Li et al. reports that CD147 regulates the lipid metabolism in cancer cells (20).

Making cancer fat: reprogramming of lipid metabolism by CD147 in hepatocellular carcinoma