[Energy metabolism of acute myeloid leukemia cells in the bone marrow microenvironment]

In the bone marrow (BM) microenvironment, acute myeloid leukemia (AML) cells constantly regulate their metabolic state based on extracellular signaling and nutrient availability by making "decisions," such as quiescence, proliferation, and differentiation. AML cells survive by meeting the biochemical demands of increased cell proliferation and continually adapting to changes in nutrient and oxygen availability. In addition, changes in the metabolism of amino acids, which are intermediate metabolites that fuel multiple biosynthetic pathways, as well as protein components, are another modality for meeting these demands. AML cells rewire metabolic pathways to adapt to increased nutritional demands for energy, reduced equivalents, and cell biosynthesis in the BM microenvironment. Furthermore, BM stromal cells and adipocytes play a role in preventing nutrient starvation-induced apoptosis of AML cells. Therefore, targeting metabolic abnormalities in AML cells is a promising novel therapeutic approach. Thus, this review describes the metabolic and molecular mechanisms of mitochondrial oxidative phosphorylation, fatty acid oxidation, and amino acid metabolism in AML cells under the BM microenvironment.