Evidence map›Paper›PMID 31160593›Full record

ArticleNature communications2019

Targeting EZH2 histone methyltransferase activity alleviates experimental intestinal inflammation.

Jie Zhou, Shuo Huang, Zhongyu Wang, Jiani Huang, Liang Xu, Xuefeng Tang, Yisong Y Wan, Qi-Jing Li, Alistair L J Symonds, Haixia Long and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 155 citations in OpenAlex.

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27 more citing papers are in PubMed but not listed here.

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

11 authors at 5 institutions in 3 countries.

Jie ZhouInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Shuo HuangInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Zhongyu WangInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Jiani HuangInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Liang XuInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Xuefeng TangDepartment of Pathology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Yisong Y WanDepartment of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599, USA.
Qi-Jing LiDepartment of Immunology, Duke University Medical Center, Durham, 27710, North Carolina, USA.
Alistair L J SymondsInstitute of Cell and Molecular Science, Barts and London School of Medicine and Dentistry, University of London, London, E1 2AT, UK.
Haixia LongInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China. longhaixialhx@163.com.
Bo ZhuInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China. bo.zhu@tmmu.edu.cn.
Army Medical University · CNXinqiao Hospital · CNDuke University Hospital · USQueen Mary University of London · GBUniversity of North Carolina at Chapel Hill · US

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81222031National Natural Science Foundation of China (National Science Foundation of China) 81773031National Natural Science Foundation of China (National Science Foundation of China) 81802865
6 · The paper itself

Abstract

Enhancer of zeste homolog 2 (EZH2)-mediated trimethylation of histone 3 lysine 27 (H3K27Me3) is critical for immune regulation. However, evidence is lacking to address the effect of EZH2 enzyme's activity on intestinal immune responses during inflammatory bowel disease (IBD). Here we report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In addition, we identified an increased number of functional MDSCs in the colons, which are essential for EZH2 inhibitor activity. Moreover, inhibition of EZH2 activity promotes the generation of MDSCs from hematopoietic progenitor cells in vitro, demonstrating a previously unappreciated role for EZH2 in the development of MDSCs. Together, these findings suggest the feasibility of EZH2 inhibitor clinical trials for the control of IBD. In addition, this study identifies MDSC-promoting effects of EZH2 inhibitors that may be undesirable in other therapeutic contexts and should be addressed in a clinical trial setting.

Indexed as

AnimalsCell DifferentiationColitisColonColonic NeoplasmsDextran SulfateEnhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsFemaleHematopoietic Stem CellsHistone CodeHistonesIndazolesIndolesInflammatory Bowel DiseasesIn Vitro TechniquesDextran SulfateEnhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsEzh2 protein, mouseGSK-2816126GSK343HistonesIndazolesIndolesPyridones

Identifiers

PMID31160593
PMCPMC6547712
OpenAlexW2948655969

What OpenQuestion holds

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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.