Evidence map›Paper›PMID 20087897›Full record

ArticleThe Prostate2010

Comprehensive evaluation of the role of EZH2 in the growth, invasion, and aggression of a panel of prostate cancer cell lines.

Breanne D W Karanikolas, Marxa L Figueiredo, Lily Wu

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Breanne D W KaranikolasDepartment of Molecular and Medical Pharmacology, Institute of Molecular Medicine, University of California Los Angeles, Los Angeles, California 90095-1738, USA.
Marxa L Figueiredo
Lily Wu
University of California, Los Angeles · USLouisiana State University · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
UCLA SPORE IN PROSTATE CANCERP50CA092131 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FREEMAN, MICHAEL R · 2002 to 2023
$42.6M
Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ANTON, PETER A · 1991 to 2018
$39.9M
Gene-Based Imaging and Therapy To Target Prostate CancerR01CA101904 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WU, LILY · 2003 to 2012
$2.9M
NCI NIH HHS P30 CA016042NCI NIH HHS P50 CA092131NCI NIH HHS R01 CA101904NIAID NIH HHS P30 AI028697
6 · The paper itself

Abstract

backgroundAlthough most prostate cancers respond well to initial treatments, a fraction of prostate cancers are more aggressive and will recur and metastasize. At that point, there are few treatment options available. Significant efforts have been made to identify biomarkers that will identify these more aggressive cancers to tailor a more vigorous treatment in order to improve outcome. Polycomb Group protein enhancer of zeste 2 (EZH2) was found to be overexpressed in metastatic prostate tumors, and is considered an excellent candidate for such a biomarker. Scattered studies have found that EZH2 overexpression causes neoplastic transformation, invasion, and growth of prostate cells. However, these studies utilized different systems and cell lines, and so are difficult to correlate with one another.

methodsIn this study, a comprehensive evaluation of the phenotypic effects of EZH2 in a panel of five prostate cancer cell lines was performed. By using multiple cell lines, and examining overexpression and knockdown of EZH2 concurrently, a broad view of EZH2's role in prostate cancer was achieved.

resultsOverexpression of EZH2 led to more aggressive behaviors in all prostate cell lines tested. In contrast, downregulation of EZH2 reduced invasion and tumorigenicity of androgen-independent (AI) cell lines CWR22Rv1, PC3, and DU145, but not of androgen-dependent (AD) cell lines LAPC4 and LNCaP.

conclusionsFindings from this study suggest that AI prostate tumors are more dependent on EZH2 expression than AD tumors. Our observations provide an explanation for the strong correlation between EZH2 overexpression and advanced stage, aggressive prostate cancers.

Indexed as

Cell ProliferationAdenocarcinomaAndrogensBiomarkers, TumorCell Line, TumorDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinGene Expression Regulation, NeoplasticHumansLentivirusMaleNeoplasm InvasivenessNeoplasm StagingPhenotypePolycomb Repressive Complex 2Prostatic NeoplasmsAndrogensBiomarkers, TumorDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanPolycomb Repressive Complex 2Transcription Factors

Identifiers

PMID20087897
PMCPMC2848714
OpenAlexW2015915171

What OpenQuestion holds

Textmetadata
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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.