ArticleNucleic acids research2021
Aberrant splicing in neuroblastoma generates RNA-fusion transcripts and provides vulnerability to spliceosome inhibitors.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 32 citations in OpenAlex.
- MYCN and helicases DDX17 and DDX5 have opposite effects on the production of readthrough-associated chimeric transcripts.Cellular and molecular life sciences : CMLS · 2026Article
- Targeting TRIM59 impairs RNA splicing and promotes neuroblastoma differentiation and therapeutic responses.Journal of experimental & clinical cancer research : CR · 2025Article
- RBM39 degrader invigorates innate immunity to eradicate neuroblastoma despite cancer cell plasticity.Nature communications · 2025Article
- SRC Kinase Isoforms Regulate mRNA Splicing during Neural Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- T-DNAreader: fast and precise identification of T-DNA insertion sites in plant genomes using RNA sequencing data.Genome biology · 2025Article
- Targeting Pathways in Neuroblastoma: Advances in Treatment Strategies and Clinical Outcomes.International journal of molecular sciences · 2025Review
- SNP array analysis facilitates the identification of novel chromosomal alterations associated with disease and SNPs related to adverse drug reactions in neuroblastoma.Oncology letters · 2025Article
- Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025Review
- Spliceosomal vulnerability of MYCN-amplified neuroblastoma is contingent on PRMT5-mediated regulation of epitranscriptomic and metabolomic pathways.Cancer letters · 2024Article
- LoDEI: a robust and sensitive tool to detect transcriptome-wide differential A-to-I editing in RNA-seq data.Nature communications · 2024Article
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- Investigating SH-SY5Y Neuroblastoma Cell Surfaceome as a Model for Neuronal-Targeted Novel Therapeutic Modalities.International journal of molecular sciences · 2022Article
- A signature based on five immune-related genes to predict the survival and immune characteristics of neuroblastoma.BMC medical genomics · 2022Article
- Comprehensive analysis of spliceosome genes and their mutants across 27 cancer types in 9070 patients: clinically relevant outcomes in the context of 3P medicine.The EPMA journal · 2022Article
- Non-Canonical Splicing and Its Implications in Brain Physiology and Cancer.International journal of molecular sciences · 2022Review
- Targeting the spliceosome through RBM39 degradation results in exceptional responses in high-risk neuroblastoma models.Science advances · 2021Article
- Ral GEF with the PH Domain and SH3 Binding Motif 1 Regulated by Splicing Factor Junction Plakoglobin and Pyrimidine Metabolism Are Prognostic in Uterine Carcinosarcoma.Disease markers · 2021Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The paucity of recurrent mutations has hampered efforts to understand and treat neuroblastoma. Alternative splicing and splicing-dependent RNA-fusions represent mechanisms able to increase the gene product repertoire but their role in neuroblastoma remains largely unexplored. Here we investigate the presence and possible roles of aberrant splicing and splicing-dependent RNA-fusion transcripts in neuroblastoma. In addition, we attend to establish whether the spliceosome can be targeted to treat neuroblastoma. Through analysis of RNA-sequenced neuroblastoma we show that elevated expression of splicing factors is a strong predictor of poor clinical outcome. Furthermore, we identified >900 primarily intrachromosomal fusions containing canonical splicing sites. Fusions included transcripts from well-known oncogenes, were enriched for proximal genes and in chromosomal regions commonly gained or lost in neuroblastoma. As a proof-of-principle that these fusions can generate altered gene products, we characterized a ZNF451-BAG2 fusion, producing a truncated BAG2-protein which inhibited retinoic acid induced differentiation. Spliceosome inhibition impeded neuroblastoma fusion expression, induced apoptosis and inhibited xenograft tumor growth. Our findings elucidate a splicing-dependent mechanism generating altered gene products in neuroblastoma and show that the spliceosome is a potential target for clinical intervention.
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