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Updated: Sep 21, 2025

CD Spectroscopy to Study DNA-Protein Interactions
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The SWI/SNF ATPase BRG1 facilitates multiple pro-tumorigenic gene expression programs in SMARCB1-deficient cancer

Kylie C Moe1, Jack N Maxwell1, Jing Wang2,3

  • 1Department of Biology, Middle Tennessee State University, Murfreesboro, TN, 32132, USA.

Oncogenesis
|June 1, 2022
PubMed

Insights

Residual SWI/SNF complexes maintain malignant rhabdoid tumor (MRT) growth by facilitating MYC oncogene expression and maintaining open chromatin at AP-1-driven cancer genes. This reveals new therapeutic targets for MRT.

Area of Science:

  • Cancer Biology
  • Chromatin Remodeling
  • Epigenetics

Background:

  • Malignant rhabdoid tumor (MRT) arises from SNF5 loss in SWI/SNF complexes.
  • Residual SWI/SNF (rSWI/SNF) complexes and MYC oncogene are present in MRT.
  • The role of rSWI/SNF in MYC activity and oncogenesis is unclear.

Purpose of the Study:

  • To investigate the role of rSWI/SNF in MYC-driven oncogenesis in MRT.
  • To uncover direct links between rSWI/SNF and other oncogenes in MRT.

Main Methods:

  • Utilized a chemical degrader to deplete the SWI/SNF ATPase, BRG1.
  • Performed gene expression and chromatin accessibility assays.

Main Results:

  • Demonstrated that rSWI/SNF facilitates MYC target gene expression.
  • Showed rSWI/SNF maintains open chromatin at AP-1-associated cancer gene sites.
  • Observed that MYC target gene expression changes are not solely linked to rSWI/SNF chromatin remodeling.

Conclusions:

  • rSWI/SNF complexes contribute to MRT oncogenesis through multiple mechanisms.
  • rSWI/SNF influences MYC activity and maintains open chromatin at AP-1-driven sites.
  • This study provides insights into rSWI/SNF's role in impaired SWI/SNF function and cancer.

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