ArticleCancer research2022
Cancer-Associated SF3B1 Mutations Confer a BRCA-Like Cellular Phenotype and Synthetic Lethality to PARP Inhibitors.
Article in Cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- Serial Cell-Free DNA Sequencing inJCO precision oncology · 2024Trial
- PANoptosis in the pathogenesis of myelodysplastic syndromes.Molecular oncology · 2026Review
- A Bayesian-Based Integrative Bioinformatics Analysis Nominates Oncogenic Drivers in Neuroblastoma.Clinical and translational science · 2026Article
- Integrative CRISPR Screening and RNA Analyses Discover an Essential Role for PUF60 Interactions with 3' Splice Sites in Cancer Progression.Cancer research · 2026Article
- Cancer-associated SF3B1 mutation suppresses DNA repair by disrupting the organization of nuclear actin network.Cell death & disease · 2026Article
- Clinical application of PARP inhibitors and emerging strategies to overcome resistance: a pan-cancer perspective.Biomarker research · 2026Review
- Synthetic lethality in cancer drug discovery: challenges and opportunities.Nature reviews. Drug discovery · 2026Review
- Distinct and convergent effects ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Short Report: The Variants inJournal of clinical medicine · 2025Article
- Synthetic lethality in cancer: a protocol for scoping review of gene interactions from synthetic lethal screens and functional studies.Systematic reviews · 2025Article
- Low-risk MDS-A spotlight on precision medicine forHemaSphere · 2025Review
- The splicing machinery is dysregulated and represents a therapeutic vulnerability in breast cancer.Cellular and molecular life sciences : CMLS · 2024Article
- Molecular impact of mutations in RNA splicing factors in cancer.Molecular cell · 2024Review
- The Impact of Spliceosome Inhibition in SF3B1-Mutated Uveal Melanoma.Investigative ophthalmology & visual science · 2024Article
- Mis-splicing of Mitotic Regulators Sensitizes SF3B1-Mutated Human HSCs to CHK1 Inhibition.Blood cancer discovery · 2024Article
- New Horizons of Synthetic Lethality in Cancer: Current Development and Future Perspectives.Journal of medicinal chemistry · 2024Review
- Tumor Antigens beyond the Human Exome.International journal of molecular sciences · 2024Review
- Accelerated DNA replication fork speed due to loss of R-loops in myelodysplastic syndromes with SF3B1 mutation.Nature communications · 2024Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in SF3B1 have been identified across several cancer types. This key spliceosome component promotes the efficient mRNA splicing of thousands of genes including those with crucial roles in the cellular response to DNA damage. Here, we demonstrate that depletion of SF3B1 specifically compromises homologous recombination (HR) and is epistatic with loss of BRCA1. More importantly, the most prevalent cancer-associated mutation in SF3B1, K700E, also affects HR efficiency and as a consequence, increases the cellular sensitivity to ionizing radiation and a variety of chemotherapeutic agents, including PARP inhibitors. In addition, the SF3B1 K700E mutation induced unscheduled R-loop formation, replication fork stalling, increased fork degradation, and defective replication fork restart. Taken together, these data suggest that tumor-associated mutations in SF3B1 induce a BRCA-like cellular phenotype that confers synthetic lethality to DNA-damaging agents and PARP inhibitors, which can be exploited therapeutically. SIGNIFICANCE: The cancer-associated SF3B1K700E mutation induces DNA damage via generation of genotoxic R-loops and stalled replication forks, defective homologous recombination, and increased replication fork degradation, which can be targeted with PARP inhibitors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.