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Updated: May 5, 2026

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Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer

Anastasia Wyce1, Yan Degenhardt, Yuchen Bai

  • 1Cancer Epigenetics DPU, Oncology R and D GlaxoSmithKline, Collegeville, PA, USA.

Oncotarget
|December 3, 2013
PubMed

Insights

BET inhibitors, like I-BET762, reduce MYC oncogene expression in prostate cancer models. This targeted approach inhibits tumor growth and offers potential for solid tumor therapies.

Area of Science:

  • Molecular Biology
  • Oncology
  • Pharmacology

Background:

  • Bromodomain and extra-terminal (BET) proteins are key regulators of gene expression, particularly the MYC oncogene.
  • BET inhibitors disrupt BET protein binding to acetylated chromatin, impacting transcriptional elongation.
  • MYC is frequently overexpressed in hematologic and solid tumors, driving cancer progression.

Purpose of the Study:

  • To investigate the efficacy of the BET inhibitor I-BET762 in regulating MYC expression in prostate cancer.
  • To assess the impact of I-BET762 on prostate cancer cell growth and tumor burden in vivo.

Main Methods:

  • Utilized prostate cancer cell lines and a patient-derived tumor model.
  • Administered the specific BET inhibitor I-BET762.
  • Monitored MYC expression levels, cell proliferation, and tumor volume.

Main Results:

  • I-BET762 significantly reduced MYC expression in prostate cancer models.
  • I-BET762 inhibited cell growth in vitro and reduced tumor burden in vivo.
  • Observed that MYC down-regulation partially contributes to I-BET762's anti-cancer effects.

Conclusions:

  • I-BET762 demonstrates potent anti-tumor activity in prostate cancer models, partly via MYC inhibition.
  • Further investigation into additional mechanisms of I-BET762 action is warranted.
  • BET inhibitors represent a promising therapeutic strategy for MYC-driven solid tumors.

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