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Updated: Jun 15, 2025

Targeted and Selective Treatment of Pluripotent Stem Cell-derived Teratomas Using External Beam Radiation in a Small-animal Model
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Targeting SWI/SNF ATPases reduces neuroblastoma cell plasticity.

Man Xu1, Jason J Hong1, Xiyuan Zhang1

  • 1Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.

The EMBO Journal
|August 22, 2024
PubMed
Summary

SWI/SNF chromatin remodelers drive neuroblastoma (NB) plasticity and therapy resistance. Targeting these ATPases with degraders inhibits NB growth and prevents chemotherapy resistance by suppressing plasticity-associated gene programs.

Keywords:
Cancer Cell PlasticityCore Transcription FactorsEpigenetic PlasticityNeuroblastomaSWI/SNF Complexes

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Area of Science:

  • Epigenetics
  • Cancer Biology
  • Chromatin Remodeling

Background:

  • Neuroblastoma (NB) exhibits tumor cell heterogeneity impacting therapy response.
  • NB comprises adrenergic and mesenchymal subtypes, with mesenchymal features emerging post-chemotherapy.
  • Lineage plasticity underlies NB subtype interconversion, but mechanisms are poorly understood.

Purpose of the Study:

  • To investigate the role of SWI/SNF chromatin remodeling complex ATPases in NB lineage plasticity.
  • To evaluate the therapeutic potential of targeting SWI/SNF ATPases in neuroblastoma.

Main Methods:

  • Utilized SMARCA2/4 dual degraders to target SWI/SNF ATPases.
  • Assessed effects on NB cell proliferation, invasion, and cellular plasticity.
  • Analyzed chromatin accessibility, enhancer activity, and transcription factor binding.

Main Results:

  • SWI/SNF ATPases are crucial for establishing a mesenchymal gene-permissive chromatin state in adrenergic NB.
  • Targeting SWI/SNF ATPases with degraders inhibited NB proliferation, invasion, and plasticity.
  • SWI/SNF ATPase depletion led to compacted chromatin, reduced enhancer activity, and displaced key transcription factors.

Conclusions:

  • SWI/SNF ATPases are pivotal drivers of neuroblastoma's intrinsic plasticity and therapy resistance.
  • Targeting SWI/SNF ATPases represents a promising epigenetic strategy for combination treatments in neuroblastoma.