ArticleCommunications biology2025
P300-dependent acetylation of the FOXQ1 complex activates super-enhancers to promote colorectal cancer proliferation and metastasis.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Super-enhancer landscape regulated by CDK12 drives retinoblastoma progression.British journal of cancer · 2026Article
- Genetically targeted mTORC1 inhibitor reveals transcriptional control by nuclear mTORC1.Nature chemical biology · 2026Article
- Single-Cell Analysis Identified a Recurrent Malignant-Associated Transcriptional State in Colorectal Cancer.Cancer science · 2026Article
- Transcriptomic Profiling Reveals Isoform-Specific Regulatory Roles of miR-196A and miR-196B in Colorectal Cancer Cells.International journal of molecular sciences · 2026Article
- p300: expanding beyond acetylation to mastermind lactylation-dependent tumorigenesis.Frontiers in cell and developmental biology · 2026Review
- Advances in the study of FOXQ1: biological functions and mechanisms.Frontiers in oncology · 2025Review
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Authors and funding
15 authors.
Funding
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Abstract
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.
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Registered trials
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