Dysregulation of sphingolipid metabolism contributes to the pathogenesis of chronic myeloid leukemia.

ABSTRACT: Chronic myeloid leukemia (CML) is primarily driven by the BCR::ABL1 oncoprotein, which has potent tyrosine kinase activity. BCR::ABL1 has been shown to facilitate several metabolic processes, including glycolysis, lipid synthesis, and protein synthesis in vitro. However, the altered metabolic profile in vivo remains poorly understood. Using Scl/tTA-BCR::ABL1 mice as a model, we conducted an analysis of plasma metabolites at different stages following BCR::ABL1 induction. Metabolites involved in sphingolipid and thiamine metabolism were significantly altered at the early stage of CML, while the tricarboxylic acid (TCA) cycle metabolites were altered during disease progression. Among these metabolic changes, sphingolipid metabolism is of particular significance. Inhibition of sphingolipid me

SUBMITTER: Xie Y 

PROVIDER: S-EPMC11993578 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature