Evidence map›Paper›PMID 26888970›Full record

ArticleBiology of reproduction2016

The Polycomb Group Protein EZH2 Impairs DNA Damage Repair Gene Expression in Human Uterine Fibroids.

Qiwei Yang, Sangeeta Nair, Archana Laknaur, Nahed Ismail, Michael P Diamond, Ayman Al-Hendy

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.7field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. UTERINE FIBROIDS.Physiological reviews · 2025
    Review
  8. Review
  9. Targeting Bromodomain-Containing Protein 9 in Human Uterine Fibroid Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Article
  10. The in vivo effects of knockdown of long non-coding RNA XIST on fibroid growth and gene expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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  19. Review
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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

6 authors at 2 institutions in 1 country.

Qiwei YangDivision of Translation Research, Department of Obstetrics and Gynecology, Augusta University, Medical College of Georgia, Augusta, Georgia qyang@gru.edu.
Sangeeta NairDivision of Translation Research, Department of Obstetrics and Gynecology, Augusta University, Medical College of Georgia, Augusta, Georgia.
Archana LaknaurDivision of Translation Research, Department of Obstetrics and Gynecology, Augusta University, Medical College of Georgia, Augusta, Georgia.
Nahed IsmailClinical Microbiology Division, Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania.
Michael P DiamondDivision of Translation Research, Department of Obstetrics and Gynecology, Augusta University, Medical College of Georgia, Augusta, Georgia.
Ayman Al-HendyDivision of Translation Research, Department of Obstetrics and Gynecology, Augusta University, Medical College of Georgia, Augusta, Georgia.
Augusta University · USUniversity of Pittsburgh · US

Funding

NICHD NIH HHS HD04622811
6 · The paper itself

Abstract

Uterine fibroids are benign, smooth muscle tumors that occur in approximately 70%-80% of women by age 50 yr. The cellular and molecular mechanism(s) by which uterine fibroids (UFs) develop are not fully understood. Accumulating evidence demonstrates that several genetic abnormalities, including deletions, rearrangements, translocations, as well as mutations, have been found in UFs. These genetic anomalies suggest that low DNA damage repair capacity may be involved in UF formation. The objective of this study was to determine whether expression levels of DNA damage repair-related genes were altered, and how they were regulated in the pathogenesis of UFs. Expression levels of DNA repair-related genes RAD51 and BRCA1 were deregulated in fibroid tissues as compared to adjacent myometrial tissues. Expression levels of chromatin protein enhancer of zeste homolog 2 (EZH2) were higher in a subset of fibroids as compared to adjacent myometrial tissues by both immunohistochemistry and Western blot analysis. Treatment with an inhibitor of EZH2 markedly increased expression levels of RAD51 and BRCA1 in fibroid cells and inhibited cell proliferation paired with cell cycle arrest. Restoring the expression of RAD51 and BRCA1 by treatment with EZH2 inhibitor was dependent on reducing the enrichment of trimethylation of histone 3 lysine 27 epigenetic mark in their promoter regions. This study reveals the important role of EZH2-regulated DNA damage-repair genes via histone methylation in fibroid biology, and may provide novel therapeutic targets for the medical treatment of women with symptomatic UFs.

Indexed as

BRCA1 ProteinCell Line, TumorDNA RepairDown-RegulationEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticFemaleGene Expression RegulationHistonesHumansLeiomyomaMyometriumRad51 RecombinaseUp-RegulationBRCA1 ProteinBRCA1 protein, humanEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistonesRAD51 protein, humanRad51 RecombinaseBRCA1DNA damage repairEZH2fibroidH3K27me3RAD51

Identifiers

PMID26888970
PMCPMC4829092
OpenAlexW2284974143

What OpenQuestion holds

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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.