JQ1: a novel potential therapeutic target

Pharmazie. 2018 Sep 1;73(9):491-493. doi: 10.1691/ph.2018.8480.


The bromo- and extra-terminal domain (BET) signaling pathway plays an important role in cell proliferation, immune responses, and pro-inflammatory events. JQ1 as a first-in-class potent and selective inhibitor of the BRD4 signaling pathway is widely used for tumor biology studies. It was found that JQ1 could potently reduce cancer cell viability in vitro and in vivo. The underlying mechanisms include an effect on cell cycle arrest in the G1 phase and a decrease in the percentage of cells in the S phase. Furthermore, JQ1 could alter cytokines expressions not only in T cells but also in dendritic cells (DCs). Apoptosis of tumor cells was induced by JQ1 through downregulation of E2f1 protein expression. In addition, JQ1 exhibited a potent suppressive effect on ERα and androgen receptor (AR) signaling pathways in breast and prostate cancers. Accumulating evidence supports the notion of BRD4 suppression as a target of therapeutic intervention in clinical oncology. Our present review article advances the understanding of the role of the JQ1 / BRD4 protein.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects
  • Azepines / pharmacology*
  • Cell Cycle Checkpoints / drug effects
  • Cell Cycle Proteins
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Estrogen Receptor alpha / antagonists & inhibitors
  • Humans
  • Molecular Targeted Therapy
  • Neoplasms / drug therapy*
  • Neoplasms / pathology
  • Nuclear Proteins / antagonists & inhibitors
  • Signal Transduction / drug effects
  • Transcription Factors / antagonists & inhibitors
  • Triazoles / pharmacology*


  • (+)-JQ1 compound
  • Antineoplastic Agents
  • Azepines
  • BRD4 protein, human
  • Cell Cycle Proteins
  • ESR1 protein, human
  • Estrogen Receptor alpha
  • Nuclear Proteins
  • Transcription Factors
  • Triazoles