Skip to main content
Fig. 4 | Journal of Hematology & Oncology

Fig. 4

From: The dual role of autophagy in acute myeloid leukemia

Fig. 4

Autophagy crosstalks with tumor metabolism in AML pathogenesis. Distorted autophagy in the heterozygous loss of Atg5 protein in AML alters cell metabolism to aerobic glycolysis and enhances its aggressiveness. Decreased glycolysis and accumulation of lactate by syrosingopine (MCT4 inhibitor) inhibits cell proliferation through autophagic cell death. Glutamine depletion through L-asparaginase inhibits the mTOR pathway, strongly activating autophagy and apoptosis. AML with overexpressed FASN gene enhances mTOR signaling to sequester the transcription factor TFEB in the cytoplasm, thus blocking activities of leukemic cell differentiation. Lipid metabolism through autophagy is crucial to maintain the OXPHOS function in AML. When lipophagy is blocked, lipid droplets accumulate in AML cells, which suppress mitochondrial OXPHOS and cause cell death

Back to article page