Lipid transactions in cancer—the fat addiction and glycerol-3-phosphate acyltransferase action
Cancer is a complex-multistep process comprising genetic, molecular and metabolic events. Cancer cells are highly proliferative and invasive, always associated with an upregulation in their “natural building blocks”—nucleic acids, proteins and lipids. Due to a high genetic burden and also because of increasing structural and functional demands, a perturbation arises in the levels of numerous metabolites in biochemical pathways related to these building blocks. The metabolic signatures in cancer have been documented to reach diagnostic accuracy, serving as potential biomarkers. Metabolomics profile was explored in a wide range of cancers so far, including ovarian cancer, oesophago-gastric cancer, colorectal cancer etc, and dysregulation was noted in the pathways of cellular respiration, carbohydrate, protein, nucleotide and lipid metabolism (1). Metabolome shift is pivotal to cancer progression and among the key metabolic pathways, glucose and glutamine metabolism were widely highlighted, and phospholipid-choline metabolism are among the recently dissected candidates. The most popular metabolic change in cancer is the “Warburg effect”, characterized by heightened anaerobic glycolysis (lactic acidosis), where ATP generation is significantly obliterated. “Warburg effect” was one of the preliminary observations in cancer, but years later deviation was reported in several other pathways.