Evidence map›Paper›PMID 34301901›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

EZH2 inhibits NK cell-mediated antitumor immunity by suppressing CXCL10 expression in an HDAC10-dependent manner.

Suresh Bugide, Romi Gupta, Michael R Green, Narendra Wajapeyee

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
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  12. Killing the killers: Natural killer cell therapy targeting glioma stem cells in high-grade glioma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  13. Article
  14. Review
  15. Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025
    Review
  16. Article
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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

4 authors at 2 institutions in 1 country.

Suresh BugideDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35233.
Romi GuptaDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35233.ORCID 0000-0001-5108-5962
Michael R GreenDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605 nwajapey@uab.edu michael.green@umassmed.edu.ORCID 0000-0003-3017-3298
Narendra WajapeyeeDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35233; nwajapey@uab.edu michael.green@umassmed.edu.ORCID 0000-0003-3306-349X
University of Alabama at Birmingham · USUniversity of Massachusetts Chan Medical School · US

Funding

A Novel Druggable Epigenetic Vulnerability Pathway in HCCR01CA218008 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KELLIHER, MICHELLE ALICE, WAJAPEYEE, NARENDRA · 2018 to 2022
$2.9M
Deciphering and targeting a non-genetic driver pathway in hepatocellular carcinomaR01CA257046 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WAJAPEYEE, NARENDRA · 2021 to 2025
$2.3M
NCI NIH HHS R01 CA218008NCI NIH HHS R01 CA257046
6 · The paper itself

Abstract

Enhancer of zeste homolog 2 (EZH2) is a histone H3 lysine 27 methyltransferase that has been shown to function as an oncogene in some cancers. Previous reports have largely focused on the ability of EZH2 to regulate cell-intrinsic tumor regulatory pathways as its mechanism-of-oncogenic action. However, the role that EZH2-mediated immune suppression plays in its oncogenic activity is not fully known. In particular, the role of natural killer (NK) cells in EZH2-driven tumor growth remains incompletely understood. Here, we demonstrate that genetic or pharmacological inhibition of EZH2 induces reexpression of the chemokine CXCL10 in hepatic tumor cells. We find that histone deacetylase 10 (HDAC10) is necessary for EZH2 recruitment to the

Indexed as

AnimalsBenzopyransCarcinoma, HepatocellularCell Line, TumorCell MovementChemokine CXCL10ChemokinesDecitabineEnhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsGene Expression Regulation, NeoplasticHistone DeacetylasesHumansIndazolesIndolesKiller Cells, NaturalBenzopyransChemokine CXCL10ChemokinesCXCL10 protein, humanDecitabineEED226Enhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsEZH2 protein, humanGSK-2816126GSK343HDAC10 protein, humanHistone DeacetylasesIndazolesIndolesPhenolsPyridonesSulfonestheasinensin ATriazolesCXCL10EZH2HDAC10hepatocellular carcinomaNK cells

Identifiers

PMID34301901
PMCPMC8325240
OpenAlexW3183393571

What OpenQuestion holds

Textmetadata
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.