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Sökning: WFRF:(Incarnato Danny)

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1.
  • Ciesla, Maciej, et al. (författare)
  • m6A-driven SF3B1 translation control steers splicing to direct genome integrity and leukemogenesis
  • 2023
  • Ingår i: Molecular Cell. - : Elsevier BV. - 1097-2765 .- 1097-4164. ; 83:7, s. 11-1179
  • Tidskriftsartikel (refereegranskat)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.
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2.
  • Ciesla, Maciej, et al. (författare)
  • Oncogenic translation directs spliceosome dynamics revealing an integral role for SF3A3 in breast cancer
  • 2021
  • Ingår i: Molecular Cell. - : Elsevier BV. - 1097-2765. ; 81:7
  • Tidskriftsartikel (refereegranskat)abstract
    • Splicing is a central RNA-based process commonly altered in human cancers; however, how spliceosomal components are co-opted during tumorigenesis remains poorly defined. Here we unravel the core splice factor SF3A3 at the nexus of a translation-based program that rewires splicing during malignant transformation. Upon MYC hyperactivation, SF3A3 levels are modulated translationally through an RNA stem-loop in an eIF3D-dependent manner. This ensures accurate splicing of mRNAs enriched for mitochondrial regulators. Altered SF3A3 translation leads to metabolic reprogramming and stem-like properties that fuel MYC tumorigenic potential in vivo. Our analysis reveals that SF3A3 protein levels predict molecular and phenotypic features of aggressive human breast cancers. These findings unveil a post-transcriptional interplay between splicing and translation that governs critical facets of MYC-driven oncogenesis.
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