Evidence map›Paper›PMID 34349243›Full record

ReviewOncogene2021

Going beyond Polycomb: EZH2 functions in prostate cancer.

Su H Park, Ka-Wing Fong, Ezinne Mong, M Cynthia Martin, Gary E Schiltz, Jindan Yu

Open access · greenAbstract readReview
In one paragraph

Review in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 100 citations in OpenAlex.

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7 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

6 authors at 1 institution in 1 country.

Su H ParkDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Ka-Wing FongDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Ezinne MongDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
M Cynthia MartinDepartment of Chemistry, Northwestern University, Evanston, IL, USA.
Gary E SchiltzDepartment of Chemistry, Northwestern University, Evanston, IL, USA.
Jindan YuDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. jindan-yu@northwestern.edu.ORCID http://orcid.org/0000-0002-2326-0409
Northwestern University · US

Funding

Targeting FOXA1-downstream pathways: a novel therapeutic strategy for castration-resistant prostate cancerP50CA180995 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ABDULKADIR, SARKI A., HUSSAIN, MAHA H · 2015 to 2025
$19.9M
CARCINOGENESIS TRAINING PROGRAMT32CA009560 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathleen Janee Green · 1986 to 2026
$8.4M
Role of NF90 in Prostate CancerR01CA227918 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI YU, JINDAN · 2018 to 2022
$1.8M
NCI NIH HHS P50 CA180995NCI NIH HHS R01 CA227918NCI NIH HHS T32 CA009560
6 · The paper itself

Abstract

The Polycomb group (PcG) protein Enhancer of Zeste Homolog 2 (EZH2) is one of the three core subunits of the Polycomb Repressive Complex 2 (PRC2). It harbors histone methyltransferase activity (MTase) that specifically catalyze histone 3 lysine 27 (H3K27) methylation on target gene promoters. As such, PRC2 are epigenetic silencers that play important roles in cellular identity and embryonic stem cell maintenance. In the past two decades, mounting evidence supports EZH2 mutations and/or over-expression in a wide array of hematological cancers and solid tumors, including prostate cancer. Further, EZH2 is among the most upregulated genes in neuroendocrine prostate cancers, which become abundant due to the clinical use of high-affinity androgen receptor pathway inhibitors. While numerous studies have reported epigenetic functions of EZH2 that inhibit tumor suppressor genes and promote tumorigenesis, discordance between EZH2 and H3K27 methylation has been reported. Further, enzymatic EZH2 inhibitors have shown limited efficacy in prostate cancer, warranting a more comprehensive understanding of EZH2 functions. Here we first review how canonical functions of EZH2 as a histone MTase are regulated and describe the various mechanisms of PRC2 recruitment to the chromatin. We further outline non-histone substrates of EZH2 and discuss post-translational modifications to EZH2 itself that may affect substrate preference. Lastly, we summarize non-canonical functions of EZH2, beyond its MTase activity and/or PRC2, as a transcriptional cofactor and discuss prospects of its therapeutic targeting in prostate cancer.

Indexed as

Enhancer of Zeste Homolog 2 ProteinProstatic NeoplasmsAnimalsEpigenesis, GeneticGene Expression Regulation, NeoplasticHistonesHumansMalePolycomb Repressive Complex 2Enhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistonesPolycomb Repressive Complex 2

Identifiers

PMID34349243
PMCPMC8487936
OpenAlexW3191738745

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.