Dynamic Chromatin States Coupling with Key Transcription Factors in Colitis‐Associated Colorectal Cancer
Abstract: Inflammation is one of the critical risk factors for colorectal cancer (CRC). However, the mechanisms for transition from colitis to CRC remain elusive. Recently, epigenetic changes have emerged as important regulatory factors for colitis‐associated cancer. Here, a systematic epigenomic study of histone modifications is performed, including H3K4me1, H3K4me3, H3K27ac, H3K27me3 and H3K9me3, in an AOM‐DSS‐induced CRC mouse model. In combination with transcriptomic data, the authors generate a dataset of 105 deep sequencing files and illustrate the dynamic landscape of chromatin states at five time points during inflammation‐cancer transition. Functional gene clusters are identified based on dynamic transcriptomic and epigenomic information, and key signaling pathways in the process are illustrated. This study's results reveal that enhancer state regions play important roles during inflammation‐cancer transition. It predicts novel transcription factors based on enhancer information, and experimentally proves OTX2 as a critical tumor suppressive transcription factor. Taken together, this study provides comprehensive epigenomic data and reveals novel molecular mechanisms for colitis‐associated cancer.
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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Online-Ressource
- Language
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Englisch
- Bibliographic citation
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Dynamic Chromatin States Coupling with Key Transcription Factors in Colitis‐Associated Colorectal Cancer ; day:16 ; month:06 ; year:2022 ; extent:15
Advanced science ; (16.06.2022) (gesamt 15)
- Creator
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Chen, Lin
Luo, Zhihui
Zhao, Chen
Li, Qinglan
Geng, Yingjie
Xiao, Yong
Chen, Ming‐Kai
Li, Lianyun
Chen, Zhen‐Xia
Wu, Min
- DOI
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10.1002/advs.202200536
- URN
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urn:nbn:de:101:1-2022061715143784971988
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:23 AM CEST
Data provider
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Chen, Lin
- Luo, Zhihui
- Zhao, Chen
- Li, Qinglan
- Geng, Yingjie
- Xiao, Yong
- Chen, Ming‐Kai
- Li, Lianyun
- Chen, Zhen‐Xia
- Wu, Min
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