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BET bromodomain inhibition blocks the function of a critical AR-independent master regulator network in lethal

Daniel J Coleman1, Lina Gao1, Carly J King1,2

  • 1Knight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.

Oncogene
|April 19, 2019
PubMed

Insights

BET bromodomain inhibitors effectively suppress prostate cancer cell growth, including in castration-resistant prostate cancers (CRPC). This study identifies novel transcriptional regulators contributing to this anti-tumor activity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • BET bromodomain inhibitors suppress prostate cancer (PC) growth via c-Myc and androgen receptor (AR) pathways.
  • The role of BET inhibitors in AR-independent castration-resistant prostate cancer (CRPC) remains largely unknown.
  • Identification of additional transcriptional regulators targeted by BET inhibitors is needed.

Purpose of the Study:

  • To investigate the anti-tumor activity of BET bromodomain inhibition in diverse CRPC models.
  • To identify novel transcriptional regulators suppressed by BET inhibitors that contribute to anti-cancer effects.

Main Methods:

  • Treatment of multiple CRPC cell lines with the BET bromodomain inhibitor JQ1.
  • RNA-sequencing to analyze gene expression changes.
  • Master Regulator computational analysis to identify key transcriptional regulators.

Main Results:

  • BET bromodomain inhibition demonstrated anti-tumor activity across various CRPC models, including AR-independent and c-Myc-independent cases.
  • RNA-sequencing and Master Regulator analysis identified previously unrecognized transcriptional regulators.
  • Suppression of these regulators, through transcriptional or post-translational mechanisms, contributes to BET inhibitor efficacy.

Conclusions:

  • BET bromodomain inhibition is a promising therapeutic strategy for a broad spectrum of CRPC.
  • The study uncovers novel molecular targets and mechanisms underlying BET inhibitor action in prostate cancer.

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