Evidence map›Paper›PMID 40988026›Full record

ArticleCellular & molecular biology letters2025

FET fusion oncoproteins enrich SWI/SNF complex subtypes and interaction partners.

Malin Lindén, Lisa Andersson, Heba Albatrok, Vilma Canfjorden, Emma Jonasson, Kajsa Grönqvist, Daniel Sjövall, Pekka Jaako, Rossella Crescitelli, Henrik Fagman and 2 more

Abstract read
In one paragraph

Article in Cellular & molecular biology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Malin LindénDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-9055-2575
Lisa AnderssonDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Heba AlbatrokDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Vilma CanfjordenDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Emma JonassonDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Kajsa GrönqvistDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Daniel SjövallDepartment of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Pekka JaakoDepartment of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Rossella CrescitelliDepartment of Surgery, Institute of Clinical Sciences, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Henrik FagmanDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Pierre ÅmanDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Anders StåhlbergDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Center for Cancer Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. anders.stahlberg@gu.se.ORCID http://orcid.org/0000-0003-4243-0191

Funding

Barncancerfonden 2022-0030Barncancerfonden D2025-0003Cancerfonden 22-2080Cancerfonden 22-2470•the Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement 1006009•the Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement 965065•the Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement 966318Vetenskapsrådet 2021-01008Vetenskapsrådet 2023-02239
6 · The paper itself

Abstract

backgroundFET (FUS, EWSR1, and TAF15) fusion oncoproteins are characteristic for several sarcomas and leukemias, including myxoid liposarcoma and Ewing sarcoma. FET oncoproteins interact with the SWI/SNF chromatin remodeling complex subtypes cBAF, PBAF, and GBAF, but their impact on SWI/SNF compositions, interactions, and downstream epigenetic effects remains elusive.

methodsWe employ a comprehensive immunoprecipitation and quantitative mass spectrometry approach to determine the impact of FET oncoproteins on SWI/SNF composition and their interactomes. Validation of complex composition and interaction partners is performed by glycerol gradient sedimentation assays and co-immunofluorescence analysis. Furthermore, we determine the differential chromatin accessibility and gene regulation in FET sarcomas using assay for transposase-accessible chromatin sequencing and RNA sequencing, respectively.

resultsOur data show that FET sarcomas have distinct SWI/SNF complex compositions, with different subunit paralogs and subtype-specific components that utilize distinct sets of interaction partners, including specific transcription factors. We show that FET oncoproteins cause no major disruption of the SWI/SNF complex composition. Instead, FUS::DDIT3-bound SWI/SNF complexes in myxoid liposarcoma cells are enriched in PBAF and GBAF components as well as most interaction partners.

conclusionsThese data suggest that FET oncoproteins act together with fully assembled and functional SWI/SNF complexes and recruited interaction partners. Finally, our data reveal that the SWI/SNF compositions, interactomes, and epigenetic background contribute to the tumor type in FET sarcoma. Trial registration Clinical trial number: not applicable.

Indexed as

Chromosomal Proteins, Non-HistoneOncogene Proteins, FusionRNA-Binding Protein FUSTranscription FactorsCell Line, TumorHumansLiposarcoma, MyxoidProtein BindingRNA-Binding Protein EWSSarcoma, EwingTATA-Binding Protein Associated FactorsChromosomal Proteins, Non-HistoneEWSR1 protein, humanFUS protein, humanOncogene Proteins, FusionRNA-Binding Protein EWSRNA-Binding Protein FUSSWI-SNF-B chromatin-remodeling complexTAF15 protein, humanTATA-Binding Protein Associated FactorsTranscription FactorsEwing sarcomaFET fusion oncoproteinsMyxoid liposarcomaQuantitative mass spectrometrySWI/SNF chromatin remodeling complex

Identifiers

PMID40988026
PMCPMC12455829

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.