Evidence map›Paper›PMID 35712778›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022

Dynamic Chromatin States Coupling with Key Transcription Factors in Colitis-Associated Colorectal Cancer.

Lin Chen, Zhihui Luo, Chen Zhao, Qinglan Li, Yingjie Geng, Yong Xiao, Ming-Kai Chen, Lianyun Li, Zhen-Xia Chen, Min Wu

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Lin ChenFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Enteropathy, College of Life Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Zhihui LuoHubei Hongshan Laboratory, Hubei Key Laboratory of Agricultural Bioinformatics, College of Life Science and Technology, College of Biomedicine and Health, Interdisciplinary Sciences Institute, Huazhong Agricultural University, Wuhan, 430070, China.
Chen ZhaoFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Enteropathy, College of Life Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Qinglan LiFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Enteropathy, College of Life Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Yingjie GengHubei Hongshan Laboratory, Hubei Key Laboratory of Agricultural Bioinformatics, College of Life Science and Technology, College of Biomedicine and Health, Interdisciplinary Sciences Institute, Huazhong Agricultural University, Wuhan, 430070, China.
Yong XiaoFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Enteropathy, College of Life Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Ming-Kai ChenFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Enteropathy, College of Life Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Lianyun LiFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Enteropathy, College of Life Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Zhen-Xia ChenHubei Hongshan Laboratory, Hubei Key Laboratory of Agricultural Bioinformatics, College of Life Science and Technology, College of Biomedicine and Health, Interdisciplinary Sciences Institute, Huazhong Agricultural University, Wuhan, 430070, China.
Min WuFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Enteropathy, College of Life Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.ORCID 0000-0003-1372-4764
Wuhan University · CNHuazhong Agricultural University · CN

Funding

Foundation of Hubei Hongshan Laboratory 2021hszd002Foundation of Hubei Hongshan Laboratory 2021hszd012Foundation of Hubei Hongshan Laboratory SZYJY2021010Fundamental Research Funds for the Central UniversitiesFundamental Research Funds for the Central Universities 2662020PY001National Natural Science Foundation of China 2021ABA011National Natural Science Foundation of China 31771503National Natural Science Foundation of China 31871305National Natural Science Foundation of China 3217050383National Natural Science Foundation of China 81972647
6 · The paper itself

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.

Indexed as

ChromatinColitis-Associated NeoplasmsAnimalsHistone CodeInflammationMiceTranscription FactorsChromatinTranscription Factorschromatin statescolitis-associated cancerhistone modificationNF-κB, OTX2

Identifiers

PMID35712778
PMCPMC9376751
OpenAlexW4283073997

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.