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Inhibition of MYC by the SMARCB1 tumor suppressor

April M Weissmiller1, Jing Wang2, Shelly L Lorey1

  • 1Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, 37232, USA.

Nature Communications
|May 3, 2019
PubMed

Insights

The SWI/SNF chromatin remodeler subunit SNF5 antagonizes the MYC oncoprotein, inhibiting its DNA binding. Loss of SNF5 promotes cancer by activating MYC, revealing a novel tumor-suppressor mechanism.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • SMARCB1 encodes the SNF5 subunit of the SWI/SNF chromatin remodeler.
  • SNF5 is known to interact with the MYC oncoprotein, but its role as a coactivator is debated due to its tumor-suppressive function and MYC target gene activation upon loss.

Purpose of the Study:

  • To re-examine the relationship between MYC and SNF5.
  • To elucidate the mechanism by which SNF5 influences MYC activity and its implications in cancer.

Main Methods:

  • Biochemical assays
  • Genome-wide approaches
  • Cellular studies involving SMARCB1-null cells

Main Results:

  • SNF5 directly inhibits MYC's DNA-binding ability.
  • SNF5 impedes MYC's recognition of target genes.
  • SNF5's regulation of MYC is independent of its chromatin remodeling function.
  • Reintroducing SNF5 into SMARCB1-null cells mimics MYC inhibition effects.

Conclusions:

  • SNF5 acts as an antagonist to MYC.
  • Loss of SNF5 contributes to malignancy by promoting MYC activity.
  • This study reveals a novel tumor-suppressor role for SNF5 in antagonizing MYC.

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