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MYC Interacts with the G9a Histone Methyltransferase to Drive Transcriptional Repression and Tumorigenesis

William B Tu1, Yu-Jia Shiah2, Corey Lourenco1

  • 1Princess Margaret Cancer Centre, Toronto, ON M5G1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G1L7, Canada.

Cancer Cell
|October 10, 2018
PubMed

Insights

MYC oncogene function in cancer is clarified: MYC partners with G9a protein to repress genes, driving cancer growth. Inhibiting G9a halts MYC

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • MYC is a key oncogenic driver implicated in various cancers.
  • The precise mechanisms by which MYC contributes to malignant transformation, particularly its role in transcriptional repression, are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying MYC-mediated transcriptional repression.
  • To identify novel therapeutic targets for MYC-driven cancers by investigating MYC's interaction partners.

Main Methods:

  • Investigated the interaction between MYC and the G9a H3K9-methyltransferase complex.
  • Utilized chromatin immunoprecipitation assays to assess MYC binding.
  • Employed pharmacological inhibition of G9a in breast cancer cell lines.
  • Performed in vivo tumor growth suppression studies using genetic depletion of G9a.

Main Results:

  • Demonstrated that MYC interacts with the G9a complex to mediate transcriptional repression.
  • Showed that G9a inhibition disrupts MYC chromatin binding and leads to de-repression of target genes.
  • Identified the MYC box II region as critical for the MYC-G9a interaction.
  • Observed that G9a inhibition induces anti-proliferative responses in MYC-sensitive breast cancer cells and suppresses MYC-dependent tumor growth in vivo.

Conclusions:

  • Unveiled G9a as a crucial epigenetic regulator of MYC transcriptional repression.
  • Established the MYC-G9a interaction as a key mechanism in MYC-driven oncogenesis.
  • Highlighted G9a as a potential therapeutic vulnerability in cancers driven by MYC.
Keywords:
BioIDG9aMYCbreast cancerepigenetic therapyhistone methylationtranscriptional repression

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