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SS18::SSX and BRD9 Modulate Synovial Sarcoma Differentiation.

Anna Kuntze1, Victor Banerjee2, Marcel Trautmann1

  • 1Gerhard-Domagk-Institute of Pathology, University Hospital Münster, 48149 Münster, Germany.

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|December 24, 2025
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Summary
This summary is machine-generated.

Synovial sarcoma (SySa) is driven by SS18::SSX, which impacts BAF complexes and cell differentiation. This study reveals SS18::SSX and BRD9 regulate epithelial-mesenchymal transition (EMT) factors, influencing SySa tumor phenotype.

Keywords:
BAF complexBRD9E-CadherinEMTGBAFSS18::SSXSlugSnaildifferentiationsynovial sarcoma

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Synovial sarcoma (SySa) is a soft tissue malignancy driven by the SS18::SSX fusion protein.
  • This fusion protein affects BAF chromatin remodeling complexes, altering gene transcription and leading to tumor heterogeneity.
  • Current treatments have limited efficacy, necessitating a deeper understanding of SySa's molecular mechanisms.

Purpose of the Study:

  • To investigate the roles of SS18::SSX and specific BAF subunits in SySa differentiation.
  • To explore how these components regulate epithelial-mesenchymal transition (EMT) and associated factors.

Main Methods:

  • Nanostring analysis was used to assess gene expression changes upon silencing SS18::SSX and BRD9.
  • Published single-cell RNA sequencing data were analyzed to validate findings.
  • Focus on SS18::SSX, BRD9, EMT factors (Snail, Slug), and E-Cadherin expression.

Main Results:

  • Silencing SS18::SSX and the GBAF subunit BRD9 modulated SySa cellular differentiation pathways.
  • Both SS18::SSX and BRD9 regulate EMT-associated factors Snail and Slug.
  • SS18::SSX was identified as a repressor of E-Cadherin expression, a key EMT marker.

Conclusions:

  • SS18::SSX and BRD9 play crucial roles in regulating key EMT players in SySa.
  • These interactions provide novel insights into the multilayered regulation of tumor phenotype and potentially prognosis in SySa.
  • Understanding these mechanisms may guide the development of novel therapeutic strategies for SySa.