ArticleCell reports2025
SUGP1 loss drives SF3B1 hotspot mutant missplicing in cancer.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Outstanding Questions to Understand and Target Splicing Factor-Mutant Blood Cancers.Blood cancer discovery · 2026Article
- Unlocking the undruggable spliceosome: generative AI and structural dynamics in cancer therapy.Frontiers in cell and developmental biology · 2026Review
- G-patch proteins: important regulators of pre-mRNA splicing and ribosome biogenesis.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
SF3B1 is the most frequently mutated splicing factor in cancer. Such mutations cause missplicing by promoting aberrant 3' splice site usage; however, how this occurs mechanistically remains controversial. To address this issue, we employed a computational screen of 600 splicing-related proteins to identify those whose reduced expression recapitulates mutant SF3B1-induced splicing dysregulation. Strikingly, our analysis reveals only two proteins whose knockdown or knockout reproduces this effect. Extending our previous findings, loss of the G-patch protein SUGP1 recapitulates almost all splicing defects induced by SF3B1 hotspot mutations. Unexpectedly, loss of the RNA helicase Aquarius (AQR) reproduces ∼40% of these defects. However, we find that AQR knockdown causes significant SUGP1 missplicing and reduced SUGP1 levels, suggesting that AQR loss reproduces mutant SF3B1 splicing defects only indirectly. This study advances our understanding of missplicing caused by oncogenic SF3B1 mutations and highlights the fundamental role of SUGP1 in this process.
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