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Background <p>Triple-negative breast cancer (TNBC) is considered a highly heterogeneous disease. Androgen receptor (AR)-positive TNBC is a subtype with distinct molecular features. However, the molecular mechanism underlying the modulation of the AR signaling pathway in TNBC is still elusive.</p> Results <p>BPTF-associated protein of 18&#xa0;kDa (BAP18) was significantly upregulated in AR-positive TNBC samples and was positively correlated with advanced disease stage and poor prognosis. BAP18 was shown to act as a transcriptional corepressor of AR in AR-positive TNBC cells and is involved in the promotion of AR-positive TNBC. Mechanically, BAP18 associates with AR and the SIN3A/HDAC subcomplex. BAP18 facilitates the recruitment of SIN3A/HDAC to androgen response elements (AREs) in the promoter regions of <i>P21</i> and <i>PTEN</i>, subsequently leading to a reduced level of histone H4 acetylation on AREs.</p> Conclusion <p>Our study revealed that BAP18, which acts as a novel AR corepressor, is involved in AR-positive TNBC progression, suggesting that BAP18 could be a potential therapeutic target for AR-positive TNBC patients.</p>

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BAP18, as a corepressor of AR together with the SIN3A/HDAC complex, promotes AR-positive triple-negative breast cancer progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月29日

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  • Yiqi Zhang,
  • Zining Jin,
  • Yi Wu,
  • Xueying Tang,
  • Chunyu Wang,
  • Shengli Wang,
  • Yinlin Li,
  • Tian Zhang,
  • Feng Jin,
  • Heng Lu,
  • Yue Zhao,
  • Ang Zheng

摘要

Background

Triple-negative breast cancer (TNBC) is considered a highly heterogeneous disease. Androgen receptor (AR)-positive TNBC is a subtype with distinct molecular features. However, the molecular mechanism underlying the modulation of the AR signaling pathway in TNBC is still elusive.

Results

BPTF-associated protein of 18 kDa (BAP18) was significantly upregulated in AR-positive TNBC samples and was positively correlated with advanced disease stage and poor prognosis. BAP18 was shown to act as a transcriptional corepressor of AR in AR-positive TNBC cells and is involved in the promotion of AR-positive TNBC. Mechanically, BAP18 associates with AR and the SIN3A/HDAC subcomplex. BAP18 facilitates the recruitment of SIN3A/HDAC to androgen response elements (AREs) in the promoter regions of P21 and PTEN, subsequently leading to a reduced level of histone H4 acetylation on AREs.

Conclusion

Our study revealed that BAP18, which acts as a novel AR corepressor, is involved in AR-positive TNBC progression, suggesting that BAP18 could be a potential therapeutic target for AR-positive TNBC patients.