Drilling for Oil: Tumor-Surrounding Adipocytes Fueling Cancer

Cancer cells activate lipolysis in tumor-surrounding adipocytes leading to the release of FFAs The release of lipids also occurs through extracellular vesicles secreted by adipocytes. The tumor-derived signals that force adipocytes to deliver lipids are not fully described. Lipids are taken up by cancer cells and mainly stored as neutral lipids in lipid droplets. Cancer cells possess the ability to liberate FFAs from these stores using neutral or acid lipases. FFAs are used by cancer cells to promote tumor progression mainly through mitochondrial fatty acid oxidation that could be coupled or not to ATP production. Other mechanisms independent of mitochondrial activity have also been implicated in tumor progression. Due to defective lipolysis of bone marrow adipocytes, this metabolic symbiosis, if it exists in bone marrow, would involve different mechanisms. Over the past decade, it has become apparent that metabolic reprogramming is a key event in tumor progression. The tumor microenvironment (TME) is a source of metabolites for tumor cells. Lipid-filled mature adipocytes are frequently found in proximity to invasive human tumors and release free fatty acids (FFAs) through lipolysis. These FFAs are taken up by tumor cells and used to promote tumor progression by mechanisms that include mitochondrial fatty acid oxidation (FAO). This review discusses recent advances in our understanding of this metabolic symbiosis between adipocytes and cancer cells and underlines the differences in this metabolic crosstalk between the various types of cancer and their localization. Over the past decade, it has become apparent that metabolic reprogramming is a key event in tumor progression. The tumor microenvironment (TME) is a source of metabolites for tumor cells. Lipid-filled mature adipocytes are frequently found in proximity to invasive human tumors and release free fatty acids (FFAs) through lipolysis. These FFAs are taken up by tumor cells and used to promote tumor progression by mechanisms that include mitochondrial fatty acid oxidation (FAO). This review discusses recent advances in our understanding of this metabolic symbiosis between adipocytes and cancer cells and underlines the differences in this metabolic crosstalk between the various types of cancer and their localization.