Evidence map›Paper›PMID 27563817›Full record

ArticleOncotarget2016

EZH2 inhibition promotes epithelial-to-mesenchymal transition in ovarian cancer cells.

Horacio Cardenas, Janice Zhao, Edyta Vieth, Kenneth P Nephew, Daniela Matei

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Chromatin Organization Governs Transcriptional Response and Plasticity of Cancer Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  17. TGF-β in developmental and fibrogenic EMTs.Seminars in cancer biology · 2022
    Review
  18. Article
  19. Review
  20. Article
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

5 authors at 4 institutions in 1 country.

Horacio CardenasNorthwestern University Feinberg School of Medicine, Department of Obstetrics and Gynecology, Chicago, IL, USA.
Janice ZhaoOakland University William Beaumont School of Medicine, Rochester, MI, USA.
Edyta ViethIndiana University Department of Medicine, Indianapolis, IN, USA.
Kenneth P NephewMedical Sciences, Indiana University, Bloomington, IN, USA.
Daniela MateiNorthwestern University Feinberg School of Medicine, Department of Obstetrics and Gynecology, Chicago, IL, USA.
Northwestern University · USIndiana University Bloomington · USIndiana University – Purdue University Indianapolis · USOakland University · US

Funding

An Epigenetic Strategy for Restoring Carboplatin Sensitivity in Ovarian CancerR01CA182832 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MATEI, DANIELA E, NEPHEW, KENNETH P · 2014 to 2018
$1.6M
NCI NIH HHS R01 CA182832
6 · The paper itself

Abstract

Cancer cells acquire essential characteristics for metastatic dissemination through the process of epithelial-to-mesenchymal transition (EMT), which is regulated by gene expression and chromatin remodeling changes. The enhancer of zeste homolog 2 (EZH2), the catalytic subunit of the polycomb repressive complex 2 (PRC2), catalyzes trimethylation of lysine 27 of histone H3 (H3K27me3) to repress gene transcription. Here we report the functional roles of EZH2-catalyzed H3K27me3 during EMT in ovarian cancer (OC) cells. TGF-β-induced EMT in SKOV3 OC cells was associated with decreased levels of EZH2 and H3K27me3 (P<0.05). These effects were delayed (~72 h relative to EMT initiation) and coincided with increased (>15-fold) expression of EMT-associated transcription factors ZEB2 and SNAI2. EZH2 knockdown (using siRNA) or enzymatic inhibition (by GSK126) induced EMT-like changes in OC cells. The EMT regulator ZEB2 was upregulated in cells treated with either approach. Furthermore, TGF-β enhanced expression of ZEB2 in EZH2 siRNA- or GSK126-treated cells (P<0.01), suggesting that H3K27me3 plays a role in TGF-β-stimulated ZEB2 induction. Chromatin immunoprecipitation assays confirmed that TGF-β treatment decreased binding of EZH2 and H3K27me3 to the ZEB2 promoter (P<0.05). In all, these results demonstrate that EZH2, by repressing ZEB2, is required for the maintenance of an epithelial phenotype in OC cells.

Indexed as

Gene Expression Regulation, NeoplasticCell Line, TumorEnhancer of Zeste Homolog 2 ProteinEpithelial-Mesenchymal TransitionFemaleHistonesHumansIndolesMethylationOvarian NeoplasmsPromoter Regions, GeneticProtein BindingPyridonesRNA InterferenceTransforming Growth Factor betaZinc Finger E-box Binding Homeobox 2Enhancer of Zeste Homolog 2 ProteinEZH2 protein, humanGSK-2816126HistonesIndolesPyridonesTransforming Growth Factor betaZEB2 protein, humanZinc Finger E-box Binding Homeobox 2EMTEZH2GSK126H3K27me3ovarian cancer

Identifiers

PMID27563817
PMCPMC5356672
OpenAlexW2515268709

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.