ArticleEMBO reports2019
FET family fusion oncoproteins target the SWI/SNF chromatin remodeling complex.
Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 76 citations in OpenAlex.
- Mesenchymal tumors of the central nervous system: illustrative case.Journal of neurosurgery. Case lessons · 2026Article
- Condensates in fusion oncoprotein-driven leukemia: new biology and therapeutic opportunities.Trends in cancer · 2026Review
- FET-Rearranged Myoepithelial Tumors Are Clinically Heterogeneous and Epigenetically Distinct from PLAG1-Rearranged Adnexal and Salivary Gland Myoepithelial Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Hypoplastic acute myeloid leukemia with aberrant lymphoid antigen expression andTherapeutic advances in hematology · 2026Article
- FET fusion oncoproteins enrich SWI/SNF complex subtypes and interaction partners.Cellular & molecular biology letters · 2025Article
- Seclidemstat (SP-2577) Induces Transcriptomic Reprogramming and Cytotoxicity in Multiple Fusion-Positive Sarcomas.Cancer research communications · 2025Article
- Brain transcriptomics highlight abundant gene expression and splicing alterations in non-neuronal cells in aFTLD-U.Acta neuropathologica · 2025Article
- Subversion of mRNA degradation pathways by EWSR1::FLI1 represents a therapeutic vulnerability in Ewing sarcoma.Nature communications · 2025Article
- SWI/SNF-type complexes-transcription factor interplay: a key regulatory interaction.Cellular & molecular biology letters · 2025Review
- Mechanism of efficacy of trabectedin against myxoid liposarcoma entails detachment of the FUS-DDIT3 transcription factor from its DNA binding sites.Journal of experimental & clinical cancer research : CR · 2024Article
- Targeted RNA Sequencing of Head and Neck Adenoid Cystic Carcinoma Reveals SEC16A::NOTCH1 Fusion and MET Exon 14 Skipping as Potentially Actionable Alterations.Head and neck pathology · 2024Article
- Specific multivalent molecules boost CRISPR-mediated transcriptional activation.Nature communications · 2024Article
- Prion-like domain mediated phase separation of ARID1A promotes oncogenic potential of Ewing's sarcoma.Nature communications · 2024Article
- Seclidemstat blocks the transcriptional function of multiple FET-fusion oncoproteins.bioRxiv : the preprint server for biology · 2024Article
- Deciphering the role of FUS::DDIT3 expression and tumor microenvironment in myxoid liposarcoma development.Journal of translational medicine · 2024Article
- Heterotypic interactions can drive selective co-condensation of prion-like low-complexity domains of FET proteins and mammalian SWI/SNF complex.Nature communications · 2024Article
- Genetic, Epigenetic and Transcriptome Alterations in Liposarcoma for Target Therapy Selection.Cancers · 2024Review
- Multi-omic and functional analysis for classification and treatment of sarcomas with FUS-TFCP2 or EWSR1-TFCP2 fusions.Nature communications · 2024Article
- Epigenetic determinants of fusion-driven sarcomas: paradigms and challenges.Frontiers in cell and developmental biology · 2024Article
- EWSR1::ATF1 Orchestrates the Clear Cell Sarcoma Transcriptome in Human Tumors and a Mouse Genetic Model.Cancers · 2023Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the human FET family of RNA-binding proteins, comprising FUS, EWSR1, and TAF15, are ubiquitously expressed and engage at several levels of gene regulation. Many sarcomas and leukemias are characterized by the expression of fusion oncogenes with FET genes as 5' partners and alternative transcription factor-coding genes as 3' partners. Here, we report that the N terminus of normal FET proteins and their oncogenic fusion counterparts interact with the SWI/SNF chromatin remodeling complex. In contrast to normal FET proteins, increased fractions of FET oncoproteins bind SWI/SNF, indicating a deregulated and enhanced interaction in cancer. Forced expression of FET oncogenes caused changes of global H3K27 trimethylation levels, accompanied by altered gene expression patterns suggesting a shift in the antagonistic balance between SWI/SNF and repressive polycomb group complexes. Thus, deregulation of SWI/SNF activity could provide a unifying pathogenic mechanism for the large group of tumors caused by FET fusion oncoproteins. These results may help to develop common strategies for therapy.
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