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Updated: Apr 17, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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BRD2 is a transcriptional coactivator of Smad3 in mediating TGF-β tumor suppressive responses

Shuai Tian1,2,3, Shuchen Gu4,5,6, Shuangwu Sun1,2,3

  • 1MOE Key Laboratory of Biosystems Homeostasis & Protection and Zhejiang Key Laboratory of Molecular Cancer Biology, Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.

Oncogene
|April 15, 2026
PubMed

Insights

Bromodomain and extraterminal (BET) protein BRD2 acts as a coactivator for Smad3, enhancing transforming growth factor-β (TGF-β) signaling. This discovery reveals BRD2

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Transforming growth factor-β (TGF-β) is a cytokine regulating crucial cellular processes like proliferation and apoptosis.
  • TGF-β signaling primarily occurs via Smad-dependent gene transcription, but regulatory mechanisms remain unclear.

Purpose of the Study:

  • To identify novel coactivators that modulate Smad transcriptional activity.
  • To elucidate the role of BRD2 in TGF-β signaling pathways.

Main Methods:

  • Co-immunoprecipitation assays to detect protein interactions.
  • Chromatin immunoprecipitation to assess Smad binding.
  • Reporter gene assays to measure transcriptional activity.

Main Results:

  • BRD2 was identified as a key transcriptional coactivator for Smad3.
  • BRD2 physically interacts with Smad3 via a novel Smad3-binding region (SBR).
  • BRD2 enhances Smad3's chromatin association and transcriptional activity, crucial for TGF-β responses.

Conclusions:

  • BRD2 is a vital modulator of TGF-β signaling, impacting tumor-suppressive functions.
  • The BRD2-Smad3 interaction presents a potential therapeutic target for TGF-β-related diseases.

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