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CD69 marks a subpopulation of acute myeloid leukemia with enhanced colony forming capacity and a unique signaling activation state. | LitMetric
In acute myeloid leukemia (AML), leukemia stem cells (LSCs) have self-renewal potential and are responsible for relapse. We previously showed that, in murine AML, CD69 expression marks an LSC-enriched subpopulation with enhanced self-renewal capacity. Here, we used CyTOF to define activated signaling pathways in LSC subpopulations in AML. Furthermore, we compared the signaling activation states of CD69 and CD36 subsets of primary human AML. The human CD69 subset expresses low levels of Ki67 and high levels of NFκB and pMAPKAPKII. Additionally, the human CD69 AML subset also has enhanced colony-forming capacity. We applied Bayesian network modeling to compare the global signaling network within the human AML subsets. We find that distinct signaling states, distinguished by NFκB and pMAPKAPKII levels, correlate with divergent functional subsets, defined by CD69 and CD36 expression, in human AML. Targeting NFκB with proteasome inhibition diminished colony formation.
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