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- W4327940010 endingPage "1179.e11" @default.
- W4327940010 startingPage "1165" @default.
- W4327940010 abstract "SF3B1 is the most mutated splicing factor (SF) in myelodysplastic syndromes (MDSs), which are clonal hematopoietic disorders with variable risk of leukemic transformation. Although tumorigenic SF3B1 mutations have been extensively characterized, the role of non-mutated wild-type SF3B1 in cancer remains largely unresolved. Here, we identify a conserved epitranscriptomic program that steers SF3B1 levels to counteract leukemogenesis. Our analysis of human and murine pre-leukemic MDS cells reveals dynamic regulation of SF3B1 protein abundance, which affects MDS-to-leukemia progression in vivo. Mechanistically, ALKBH5-driven 5' UTR m6A demethylation fine-tunes SF3B1 translation directing splicing of central DNA repair and epigenetic regulators during transformation. This impacts genome stability and leukemia progression in vivo, supporting an integrative analysis in humans that SF3B1 molecular signatures may predict mutational variability and poor prognosis. These findings highlight a post-transcriptional gene expression nexus that unveils unanticipated SF3B1-dependent cancer vulnerabilities." @default.
- W4327940010 created "2023-03-21" @default.
- W4327940010 creator A5017779628 @default.
- W4327940010 creator A5030957267 @default.
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- W4327940010 creator A5071799960 @default.
- W4327940010 creator A5078578201 @default.
- W4327940010 creator A5091096270 @default.
- W4327940010 date "2023-04-01" @default.
- W4327940010 modified "2023-10-02" @default.
- W4327940010 title "m6A-driven SF3B1 translation control steers splicing to direct genome integrity and leukemogenesis" @default.
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