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Article Abstract
N-methyladenosine (mA) is a common chemical modification for mammalian mRNA and exhibits high dynamics in various biological processes. However, dynamics of mA RNA methylome during leukemogenesis remains unknown. Here, we delineate a comprehensive mA landscape during acute myeloid leukemia (AML) development and identify PRMT6 as a key for maintaining AML stem cells. We observe an obvious change in mA methylome during leukemogenesis and find that protein arginine methyltransferase PRMT6 and mA reader IGF2BP2 maintain the function of human and murine leukemia stem cells (LSCs). Genetic deletion or pharmacological inhibition of PRMT6 damages AML development and LSC function. Mechanistically, IGF2BP2 stabilizes PRMT6 mRNA via mA-mediated manner, which catalyzes H3R2me2a and suppresses lipid transporter MFSD2A expression. PRMT6 loss upregulates MFSD2A expression that increases docosahexaenoic acid levels and impairs LSC maintenance. Collectively, our findings reveal a critical role of PRMT6-MFSD2A signaling axis in AML development and provide a therapeutic strategy for targeting LSCs.
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| http://dx.doi.org/10.1016/j.stem.2022.12.003 | DOI Listing |
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