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  3. Baf Complex-independent Gene Activation By Ss18::ssx.
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  3. Baf Complex-independent Gene Activation By Ss18::ssx.

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BAF complex-independent gene activation by SS18::SSX.

Afroditi Sotiriou1,2,3,4, Jinxiu Li5,6, Sanya Middha1,2,3,4

  • 1Soft-tissue sarcoma research group, German Cancer Research Center (DKFZ), Heidelberg, Germany.

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|February 9, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

This study shows that the oncogenic SS18::SSX fusion protein in synovial sarcoma can drive transcription independently of BAF complexes. Targeting coactivators like EP300 offers new therapeutic strategies for fusion-driven cancers.

Keywords:
ATAC-seqSS18::SSXSynovial sarcomachromatin remodelingmSWI/SNF (BAF) complexestranscription

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Synovial sarcoma is driven by the SS18::SSX fusion protein, which alters BAF complex function.
  • BAF complexes are thought to be essential for SS18::SSX-driven gene activation.

Purpose of the Study:

  • To investigate the requirement of BAF activity for synovial sarcoma cell survival and SS18::SSX transcription.
  • To identify alternative mechanisms of SS18::SSX-mediated oncogenic transcription.

Main Methods:

  • Targeted degradation and genetic deletion of BAF subunits.
  • Analysis of SS18::SSX target gene expression.
  • Use of domain-specific SS18::SSX mutants.
  • Pharmacologic inhibition of EP300/CREBBP.

Main Results:

  • BAF complex loss had minimal impact on sarcoma cell viability and SS18::SSX target gene expression.
  • SS18::SSX activates transcription independently of BAF, relying on its C-terminal QPGY-rich domain.
  • SS18::SSX interacts with EP300 to promote transcription.
  • EP300/CREBBP inhibition suppressed SS18::SSX-driven transcription and reduced cell survival.

Conclusions:

  • BAF activity is not essential for SS18::SSX-mediated transcriptional activation in synovial sarcoma.
  • Synovial sarcoma relies on coactivator recruitment (e.g., EP300) for oncogenic transcription, independent of BAF.
  • Targeting EP300/CREBBP represents a potential therapeutic strategy for synovial sarcoma and other fusion-driven cancers.