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BAF155 methylation drives metastasis by hijacking super-enhancers and subverting anti-tumor immunity

Eui-Jun Kim1,2, Peng Liu3,2, Shengjie Zhang1

  • 1McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA.

Nucleic Acids Research
|December 5, 2021
PubMed

Insights

Methylation of BAF155 by CARM1 drives triple-negative breast cancer metastasis by activating oncogenes and suppressing immune responses. Inhibiting this methylation may enhance immunotherapy efficacy.

Area of Science:

  • Epigenetics
  • Cancer Biology
  • Immunology

Background:

  • SWI/SNF chromatin remodeler subunits are frequently disrupted in cancer.
  • The role of post-translational modifications (PTMs) in SWI/SNF-driven epigenetic dysfunction is largely unknown.
  • Arginine-methylation of BAF155 by CARM1 is implicated in triple-negative breast cancer (TNBC) metastasis.

Purpose of the Study:

  • To elucidate the dual roles of methylated BAF155 (me-BAF155) in promoting tumor metastasis.
  • To investigate the therapeutic potential of inhibiting CARM1 and BAF155 methylation.

Main Methods:

  • Investigated the recruitment of BRD4 by me-BAF155.
  • Analyzed the impact of me-BAF155 on interferon signaling pathways.
  • Utilized pharmacological inhibition of CARM1 and BAF155 methylation.
  • Assessed the effects on cytotoxic T cell activity and tumor infiltration.
  • Detected me-BAF155 in circulating tumor cells.

Main Results:

  • Methylated BAF155 activates super-enhancer-addicted oncogenes via BRD4 recruitment.
  • Methylated BAF155 represses interferon signaling, suppressing host immune response.
  • CARM1 inhibition abrogated oncogene expression and boosted anti-tumor immunity.
  • CARM1 inhibitors reduced TNBC cell migration, growth, and metastasis in vivo.

Conclusions:

  • Arginine methylation of BAF155 is a novel mechanism driving epigenetic dysregulation and cancer metastasis.
  • Targeting me-BAF155 presents a therapeutic strategy to enhance immunotherapy efficacy in TNBC.

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