Evidence map›Paper›PMID 27239242›Full record

ReviewClinical epigenetics2016

Polycomb repressive complex's evolutionary conserved function: the role of EZH2 status and cellular background.

Koraljka Gall Trošelj, Renata Novak Kujundzic, Djurdjica Ugarkovic

Open access · goldAbstract readReview
In one paragraph

Review in Clinical epigenetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
6.8field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Recent Advances in Renal Medullary Carcinoma.International journal of molecular sciences · 2022
    Review
  10. Epigenetic remodelling in human hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2022
    Review
  11. Review
  12. Epigenome plasticity in plants.Nature reviews. Genetics · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Potential role for EZH2 in promotion of asthma through suppression of miR-34b transcription by inhibition of FOXO3.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  17. Article
  18. Article
  19. Article
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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 1 institution in 1 country.

Koraljka Gall TrošeljDivision of Molecular Medicine, Laboratory for Epigenomics, Rudjer Boskovic Institute, Bijenicka cesta 54, 10 000 Zagreb, Croatia.
Renata Novak KujundzicDivision of Molecular Medicine, Laboratory for Epigenomics, Rudjer Boskovic Institute, Bijenicka cesta 54, 10 000 Zagreb, Croatia.
Djurdjica UgarkovicDivision of Molecular Biology, Laboratory for Evolutionary Genetics, Rudjer Boskovic Institute, Bijenicka cesta 54, 10 000 Zagreb, Croatia.
Rudjer Boskovic Institute · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

When assembled in multiprotein polycomb repressive complexes (PRCs), highly evolutionary conserved polycomb group (PcG) proteins epigenetically control gene activity. Although the composition of PRCs may vary considerably, it is well established that the embryonic ectoderm development (EED) 1, suppressor of zeste (SUZ) 12, and methyltransferase enhancer of zeste (EZH2)-containing complex, PRC2, which is abundant in highly proliferative cells (including cancer cells), establishes a repressive methylation mark on histone 3 (H3K27me3). From the perspective of molecular cancer pathogenesis, this effect, when directed towards a promoter of tumor suppressor genes, represents pro-tumorigenic effect. This mode of action was shown in several cancer models. However, EZH2 function extends beyond this scenario. The highly specific cellular background, related to the origin of cell and numerous external stimuli during a given time-window, may be the trigger for EZH2 interaction with other proteins, not necessarily histones. This is particularly relevant for cancer. This review provides a critical overview of the evolutional importance of PRC and discusses several important aspects of EZH2 functioning within PRC. The review also deals with mutational studies on EZH2. Due to the existence of several protein (and messenger RNA (mRNA)) isoforms, these mutations were stratified, using the protein sequence which is considered canonical. This approach showed that there is an urgent need for the uniformed positioning of currently known EZH2 mutations (somatic-in tumors, as well as germline mutations in the Weaver's syndrome). Finally, we discuss EZH2 function with respect to amount of trimethylated H3K27, in a specific cellular milieu, through presenting the most recent data related to EZH2-H3K27m3 relationship in cancer. All these points are significant in considering EZH2 as a therapeutic target.

Indexed as

Enhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticHistonesHumansMutationNeoplasmsPolycomb Repressive Complex 2Enhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistonesPolycomb Repressive Complex 2CancerEvolutionEZH2H3K27me3MutationPolycomb repressive complexes 1–4

Identifiers

PMID27239242
PMCPMC4882774
OpenAlexW2402046911

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.