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<p>The FOX transcription factor family plays a pivotal role in the malignant progression of tumors. We propose a hypothesis that FOXQ1 recruits p300 and BRD4 to super-enhancer regions. Our findings indicate that p300 acetylates Lys190 of FOXQ1, resulting in its recognition and binding by BRD4. Subsequently, BRD4 recruits RNA-Pol II to form a “FOXQ1-p300-BRD4-RNA Pol II” complex, which then binds to the super-enhancers of target genes. Meanwhile, acetylation at Lys190 of FOXQ1 directly enhances its binding affinity to super-enhancers. Consequently, more target oncogenes can be transcribed to promote CRC proliferation and metastasis. Our results suggest that FOXQ1 acts as a key regulator of super-enhancers, providing insights into its role in CRC and highlighting its potential as a therapeutic target.</p>

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P300-dependent acetylation of the FOXQ1 complex activates super-enhancers to promote colorectal cancer proliferation and metastasis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月7日

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  • Wen-Dong Yang,
  • Zhi-Heng Zhang,
  • Man-Yi Zhao,
  • Ke Shao,
  • Yan-Feng Ma,
  • Qi Shen,
  • Meng-Ru Lu,
  • Zhi-Ying Shao,
  • Jia-Yu Xu,
  • Meng-Han Cao,
  • Seng Meng,
  • Su-Fang Chu,
  • Hong-Mei Yong,
  • Jin Ding,
  • Jin Bai

摘要

The FOX transcription factor family plays a pivotal role in the malignant progression of tumors. We propose a hypothesis that FOXQ1 recruits p300 and BRD4 to super-enhancer regions. Our findings indicate that p300 acetylates Lys190 of FOXQ1, resulting in its recognition and binding by BRD4. Subsequently, BRD4 recruits RNA-Pol II to form a “FOXQ1-p300-BRD4-RNA Pol II” complex, which then binds to the super-enhancers of target genes. Meanwhile, acetylation at Lys190 of FOXQ1 directly enhances its binding affinity to super-enhancers. Consequently, more target oncogenes can be transcribed to promote CRC proliferation and metastasis. Our results suggest that FOXQ1 acts as a key regulator of super-enhancers, providing insights into its role in CRC and highlighting its potential as a therapeutic target.