Evidence map›Paper›PMID 18806826›Full record

ArticleOncogene2008

Repression of E-cadherin by the polycomb group protein EZH2 in cancer.

Q Cao, J Yu, S M Dhanasekaran, J H Kim, R-S Mani, S A Tomlins, R Mehra, B Laxman, X Cao, J Yu and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 330 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
330citing papers in PubMed, 2 pooled it
12.0field-weighted citation impact, top 1% 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

330 citing papers in PubMed, 2 syntheses or guidelines pooled it, 605 citations in OpenAlex.

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  15. CBX2 suppresses interferon signaling to diminish tumor immunogenicity via a noncanonical corepressor complex.Proceedings of the National Academy of Sciences of the United States of America · 2025
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270 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

13 authors at 3 institutions in 1 country.

Q CaoMichigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-0602, USA.
J Yu
S M Dhanasekaran
J H Kim
R-S Mani
S A Tomlins
R Mehra
B Laxman
X Cao
J Yu
C G Kleer
S Varambally
A M Chinnaiyan
Michigan Center for Translational Pathology · USUniversity of Michigan–Ann Arbor · USHoward Hughes Medical Institute · US

Funding

VACCINIA PSA FOR ANDROGEN-MODULATED POST-SURGICAL RECURRENCE OF PROSTATE CANCERP50CA069568 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COONEY, KATHLEEN A · 1995 to 2013
$31.3M
Epitomic Biomarkers of Prostate CancerU01CA111275 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHINNAIYAN, ARUL M, RUBIN, MARK A. · 2004 to 2015
$6.8M
Role of EZH2 in Breast Cancer ProgressionR01CA107469 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Celina G Kleer · 2005 to 2026
$5.9M
The Role of Polycomb Group Proteins in Prostate CancerR01CA097063 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHINNAIYAN, ARUL M · 2002 to 2007
$1.4M
The Role of beta-adrenergic Signaling in Prostate CancerK99CA129565 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI YU, JINDAN · 2008 to 2009
$310k
NCI NIH HHS K99 CA129565NCI NIH HHS P50 CA069568NCI NIH HHS P50 CA69568NCI NIH HHS R01 CA097063NCI NIH HHS R01 CA107469NCI NIH HHS R01 CA97063NCI NIH HHS U01 CA111275
6 · The paper itself

Abstract

Enhancer of zeste homolog 2 (EZH2) is a critical component of the polycomb-repressive complex 2 (PRC2), which is involved in gene silencing and histone H3 lysine 27 methylation. EZH2 has a master regulatory function in controlling such processes as stem cell differentiation, cell proliferation, early embryogenesis and X chromosome inactivation. Although benign epithelial cells express very low levels of EZH2, increased levels of EZH2 have been observed in aggressive solid tumors such as those of the prostate, breast and bladder. The mechanism by which EZH2 mediates tumor aggressiveness is unclear. Here, we demonstrate that EZH2 mediates transcriptional silencing of the tumor suppressor gene E-cadherin by trimethylation of H3 lysine 27. Histone deacetylase inhibitors can prevent EZH2-mediated repression of E-cadherin and attenuate cell invasion, suggesting a possible mechanism that may be useful for the development of therapeutic treatments. Taken together, these observations provide a novel mechanism of E-cadherin regulation and establish a functional link between dysregulation of EZH2 and repression of E-cadherin during cancer progression.

Indexed as

Gene Expression Regulation, NeoplasticBreast NeoplasmsCadherinsCell Line, TransformedCell Line, TumorDNA-Binding ProteinsDNA MethylationEnhancer of Zeste Homolog 2 ProteinFemaleGene SilencingHistonesHumansMaleNeoplasm InvasivenessNeoplasmsPolycomb-Group ProteinsCadherinsDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistonesPolycomb-Group ProteinsPolycomb Repressive Complex 2Repressor ProteinsTranscription Factors

Identifiers

PMID18806826
PMCPMC2690514
OpenAlexW1977090021

What OpenQuestion holds

Textmetadata
LicenceTDM
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.