Inducible in vivo silencing of Brd4 identifies potential toxicities of sustained BET protein inhibition

Cell Rep. 2014 Sep 25;8(6):1919-1929. doi: 10.1016/j.celrep.2014.08.025. Epub 2014 Sep 18.

Abstract

BET family proteins are novel therapeutic targets for cancer and inflammation and represent the first chromatin readers against which small-molecule inhibitors have been developed. First-generation BET inhibitors have shown therapeutic efficacy in preclinical models, but the consequences of sustained BET protein inhibition in normal tissues remain poorly characterized. Using an inducible and reversible transgenic RNAi mouse model, we show that strong suppression of the BET protein Brd4 in adult animals has dramatic effects in multiple tissues. Brd4-depleted mice display reversible epidermal hyperplasia, alopecia, and decreased cellular diversity and stem cell depletion in the small intestine. Furthermore, Brd4-suppressed intestines are sensitive to organ stress and show impaired regeneration following irradiation, suggesting that concurrent Brd4 suppression and certain cytotoxic therapies may induce undesirable synergistic effects. These findings provide important insight into Brd4 function in normal tissues and, importantly, predict several potential outcomes associated with potent and sustained BET protein inhibition.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Azepines / pharmacology
  • Bone Marrow Cells / metabolism
  • Cell Line
  • Doxorubicin / toxicity
  • Gamma Rays
  • Hyperplasia / pathology
  • Intestinal Mucosa / metabolism
  • Intestines / drug effects
  • Intestines / radiation effects
  • Mice
  • Mice, Transgenic
  • MicroRNAs / metabolism
  • Nuclear Proteins / antagonists & inhibitors
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • RNA Interference
  • RNA, Small Interfering / metabolism
  • Receptors, G-Protein-Coupled / metabolism
  • Skin / pathology
  • Stem Cells / cytology
  • Stem Cells / metabolism
  • Thymus Gland / metabolism
  • Transcription Factors / antagonists & inhibitors
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Triazoles / pharmacology

Substances

  • (+)-JQ1 compound
  • Azepines
  • Brd4 protein, mouse
  • Lgr5 protein, mouse
  • MicroRNAs
  • Nuclear Proteins
  • RNA, Small Interfering
  • Receptors, G-Protein-Coupled
  • Transcription Factors
  • Triazoles
  • Doxorubicin