ArticleNature communications2021
SON drives oncogenic RNA splicing in glioblastoma by regulating PTBP1/PTBP2 switching and RBFOX2 activity.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 48 citations in OpenAlex.
- The periphery of nuclear speckles defines a spatially and temporally regulated compartment of long-lived intron-retained RNAs that resolves during mitosis.Nature cell biology · 2026Article
- Review
- PTBP1 knockdown reprograms glioma stem cells into neuronal-like cells and suppresses tumorigenesis via the DUSP5-ERK1/2 signaling pathway.Neuro-oncology · 2026Article
- Metaproteomic profiling reveals viral proteins and associated host proteomic alterations in glioblastoma.Scientific reports · 2026Article
- Single-cell transcriptomics profiling elucidates RBP-driven metastatic signaling pathways in ERiScience · 2026Article
- Unravelling the role of PANoptosis in diseases: from emerging molecular mechanisms-to-therapeutic implications.Cancer biology & medicine · 2026Review
- PTBP1 inhibition reprograms myogenesis to rescue impaired muscle regeneration in mdx mice through correcting E2A splicing.Nature communications · 2026Article
- Cancer neuroscience: signaling pathways and new therapeutic strategies for cancer.Signal transduction and targeted therapy · 2026Review
- PTBP1-mediated inhibition of circular RNA SCMH1 biogenesis impairs brain recovery after ischemic stroke.Theranostics · 2026Article
- G-patch proteins: important regulators of pre-mRNA splicing and ribosome biogenesis.Frontiers in cell and developmental biology · 2026Review
- Disrupted Alternative Splicing of RAB11FIP3 Contributes to Diabetic Foot Ulcer Dysfunction.Journal of cellular and molecular medicine · 2025Article
- Temporal dynamics of the multi-omic response reveals the modulation of macrophage subsets post-myocardial infarction.Journal of translational medicine · 2025Article
- Construction of a Prognostic Model Using RNA Processing Factor Genes and the Key Role of NSUN6 in Glioma Outcomes.Journal of cellular and molecular medicine · 2025Article
- SON-dependent nuclear speckle rehabilitation alleviates proteinopathies.bioRxiv : the preprint server for biology · 2025Article
- PTBP2 promotes cell survival and autophagy in chronic myeloid leukemia by stabilizing BNIP3.Cell death & disease · 2025Article
- The emerging roles of aberrant alternative splicing in glioma.Cell death discovery · 2025Review
- Ribosome biogenesis-related gene signature predicts prognosis and immune landscape in glioma and identifies UTP20 as a therapeutic target.Frontiers in immunology · 2025Article
- SON is an essential RNA splicing factor promoting ErbB2 and ErbB3 expression in breast cancer.British journal of cancer · 2024Article
- PTBP1 as a potential regulator of disease.Molecular and cellular biochemistry · 2024Review
- Comprehensive machine learning-based integration develops a novel prognostic model for glioblastoma.Molecular therapy. Oncology · 2024Article
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
While dysregulation of RNA splicing has been recognized as an emerging target for cancer therapy, the functional significance of RNA splicing and individual splicing factors in brain tumors is poorly understood. Here, we identify SON as a master regulator that activates PTBP1-mediated oncogenic splicing while suppressing RBFOX2-mediated non-oncogenic neuronal splicing in glioblastoma multiforme (GBM). SON is overexpressed in GBM patients and SON knockdown causes failure in intron removal from the PTBP1 transcript, resulting in PTBP1 downregulation and inhibition of its downstream oncogenic splicing. Furthermore, SON forms a complex with hnRNP A2B1 and antagonizes RBFOX2, which leads to skipping of RBFOX2-targeted cassette exons, including the PTBP2 neuronal exon. SON knockdown inhibits proliferation and clonogenicity of GBM cells in vitro and significantly suppresses tumor growth in orthotopic xenografts in vivo. Collectively, our study reveals that SON-mediated RNA splicing is a GBM vulnerability, implicating SON as a potential therapeutic target in brain tumors.
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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.