ArticlebioRxiv : the preprint server for biology2026
BAF complex-independent gene activation by SS18::SSX.
Afroditi Sotiriou, Jinxiu Li, Sanya Middha, Jake A Ward, Selina Troester, Lianghao Mao, Martin Schneider, Dario Frey, Eliza C Wray, Sara Bocedi and 11 more
Abstract readPreprint
In one paragraphArticle in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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1 · What the graph read from itWhat it found
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2 · The registryThe trial behind it
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
21 authors.
Afroditi SotiriouSoft-tissue sarcoma research group, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0002-4534-7185 Jinxiu LiDepartment of Orthopaedics, University of Utah, Salt Lake City, Utah, United States of America.
Sanya MiddhaSoft-tissue sarcoma research group, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Jake A WardInstitute for Research in Biomedicine (IRB Barcelona), the Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Selina TroesterInstitute for Research in Biomedicine (IRB Barcelona), the Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0001-6268-4442 Lianghao MaoResearch Group Proteomics and Cancer Cell Signaling, Hopp Children's Cancer Center Heidelberg (KiTZ) and DKFZ, Heidelberg, Germany. Department of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg.ORCID 0009-0007-0946-6420 Martin SchneiderProteomics Core Facility, German Cancer Research Center, (DKFZ), Heidelberg, Germany.
Eliza C WrayInstitute of Genetics and Cancer, University of Edinburgh, Edinburgh, United Kingdom.
Sara BocediInstitute of Genetics and Cancer, University of Edinburgh, Edinburgh, United Kingdom.
Kyllie Smith-FryDepartment of Orthopaedics, University of Utah, Salt Lake City, Utah, United States of America.
Linda MorrisonDepartment of Orthopaedics, University of Utah, Salt Lake City, Utah, United States of America.
Lara CarrollDepartment of Orthopaedics, University of Utah, Salt Lake City, Utah, United States of America.ORCID 0000-0002-8232-7386 Ashok Kumar JayaveluResearch Group Proteomics and Cancer Cell Signaling, Hopp Children's Cancer Center Heidelberg (KiTZ) and DKFZ, Heidelberg, Germany. Department of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg.ORCID 0000-0002-3292-1117 Cristina Mayor-RuizInstitute for Research in Biomedicine (IRB Barcelona), the Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0001-6442-5495 Bradley R CairnsDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.ORCID 0000-0002-9864-8811 Kevin B JonesDepartment of Orthopaedics, University of Utah, Salt Lake City, Utah, United States of America.ORCID 0000-0003-1531-2157 Nezha S BenabdallahInstitute of Genetics and Cancer, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0001-6925-826X Ana BanitoSoft-tissue sarcoma research group, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0003-2188-0003 Funding
UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6MTargeting SS18-SSX biology in synovial sarcomagenesisU54CA231652 · NCI · UNIVERSITY OF UTAH · PI JONES, KEVIN BRUCE · 2018 to 2022
$12.0MNCI NIH HHS P30 CA042014NCI NIH HHS U54 CA231652
6 · The paper itselfAbstract
In synovial sarcoma, the BAF subunit SS18 is fused to SSX, a transcriptional repressor, generating the oncogenic SS18::SSX fusion protein. Incorporation of SS18::SSX into BAF complexes leads to their aberrant retargeting to Polycomb-repressed genes via SSX, while simultaneously altering their composition and activity. The presence of BAF at Polycomb target sites is widely assumed to be essential for gene activation. Here, we directly tested the requirement for BAF activity in synovial sarcoma cell survival and SS18::SSX-driven transcription. Using targeted degradation of BAF ATPase subunits and deletion of core components, we show that BAF loss has modest effects on sarcoma cell viability and does not impede SS18::SSX target gene expression. Consistently, deletion of the BAF ATPase subunit
Indexed as
ATAC-seqchromatin remodelingmSWI/SNF (BAF) complexesSS18::SSXSynovial sarcomatranscription
Identifiers
PMID41659547
PMCPMC12873962
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