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Tumor suppressor bromodomain-containing protein 7 cooperates with Smads to promote transforming growth factor-β

Ting Liu1,2, Meiling Zhao1, Jinquan Liu1

  • 1Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, Zhejiang 310058, China.

Oncogene
|June 9, 2016
PubMed

Insights

Bromodomain-containing protein 7 (BRD7) acts as a novel coactivator for Smad proteins in transforming growth factor-β (TGF-β) signaling. BRD7 enhances TGF-β-mediated gene transcription and cellular responses, highlighting its role in TGF-β pathway regulation.

Area of Science:

  • Cellular biology
  • Molecular signaling
  • Cancer research

Background:

  • Smad proteins are key mediators of the transforming growth factor-β (TGF-β) signaling pathway.
  • TGF-β signaling regulates crucial cellular processes including proliferation, differentiation, and apoptosis.
  • Dysregulation of TGF-β signaling is implicated in various diseases, including cancer.

Purpose of the Study:

  • To investigate the novel function of bromodomain-containing protein 7 (BRD7) in TGF-β signaling.
  • To elucidate the mechanism by which BRD7 interacts with Smad proteins and influences their transcriptional activity.
  • To determine the role of BRD7 in TGF-β-mediated cellular responses, such as tumor suppression and epithelial-mesenchymal transition.

Main Methods:

  • Co-immunoprecipitation assays to detect protein complex formation between BRD7 and Smad proteins.
  • Chromatin immunoprecipitation (ChIP) to assess Smad-chromatin association.
  • Western blotting and quantitative real-time PCR to analyze gene expression and protein levels.
  • Functional assays including cell proliferation, migration, and apoptosis assays.

Main Results:

  • BRD7 forms a TGF-β-inducible complex with Smad3/4 via its N-terminal Smad-binding domain.
  • BRD7 binds to acetylated histones and interacts with p300, a histone acetyltransferase, to enhance Smad transcriptional activity.
  • Ectopic expression of BRD7 potentiates TGF-β-induced transcriptional responses, tumor suppression, and epithelial-mesenchymal transition.
  • Depletion of BRD7 impairs TGF-β signaling pathway activity and its downstream cellular effects.

Conclusions:

  • BRD7 functions as a novel transcription coactivator for Smad proteins in the canonical TGF-β signaling pathway.
  • BRD7 integrates Smad signaling with epigenetic machinery by interacting with acetylated histones and p300.
  • BRD7 plays a critical role in mediating TGF-β-dependent physiological responses, including tumor suppression and epithelial-mesenchymal transition, making it a potential therapeutic target.

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