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Published on: May 15, 2019

BET bromodomain inhibition as a therapeutic strategy to target c-Myc

Jake E Delmore1, Ghayas C Issa, Madeleine E Lemieux

  • 1Department of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, USA.

Cell
|September 6, 2011
PubMed

Insights

Targeting MYC transcription via bromodomain inhibition with JQ1 effectively downregulates Myc-dependent genes. This approach shows therapeutic promise for multiple myeloma and other cancers driven by MYC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • The MYC oncogene drives many human cancers, but direct therapeutic strategies remain elusive.
  • MYC's role in cancer pathogenesis necessitates novel approaches to target its oncogenic functions.

Purpose of the Study:

  • To investigate the potential of inhibiting bromodomain proteins, which regulate transcription, as a strategy to modulate MYC activity.
  • To evaluate the efficacy of the small-molecule bromodomain inhibitor JQ1 in targeting MYC transcription and its downstream effects.

Main Methods:

  • Utilized JQ1, a selective bromodomain inhibitor, to target BET bromodomain proteins involved in transcriptional regulation.
  • Assessed the impact of BET inhibition on MYC transcription and genome-wide Myc-dependent gene expression.
  • Evaluated the antiproliferative effects of JQ1 in experimental models of multiple myeloma.

Main Results:

  • JQ1 selectively inhibits BET bromodomain proteins, leading to downregulation of MYC transcription.
  • Genome-wide analysis revealed broad downregulation of Myc-dependent genes following BET inhibition.
  • In multiple myeloma models, JQ1 demonstrated potent antiproliferative effects, inducing cell-cycle arrest and senescence.

Conclusions:

  • BET bromodomain proteins are critical regulators of MYC transcription.
  • JQ1 effectively targets MYC-driven transcription and exhibits therapeutic potential in preclinical models of multiple myeloma.
  • BET bromodomain inhibition represents a promising therapeutic strategy for MYC-driven malignancies.

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