Evidence map›Paper›PMID 37664059›Full record

ReviewFrontiers in oncology2023

Non-canonical functions of EZH2 in cancer.

Sarah M Zimmerman, Phyo Nay Lin, George P Souroullas

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 30 citations in OpenAlex.

  1. EZH2 Inhibition and Myeloid Risk: A Feature of On-Target Biology.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Review
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  13. Dual Effect ofBiology · 2026
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  19. Hemizygous mutation ofAmerican journal of physiology. Cell physiology · 2025
    Article
  20. Review
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.

Sarah M ZimmermanDepartment of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO, United States.
Phyo Nay LinDepartment of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO, United States.
George P SouroullasDepartment of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO, United States.
Molecular Oncology (United States) · USWashington University in St. Louis · US

Funding

MOLECULAR ONCOLOGY TRAINING GRANTT32CA113275 · NCI · WASHINGTON UNIVERSITY · PI Matthew J Walter · 2006 to 2026
$5.7M
Investigate the effect of oncogenic EZH2 mutations on chromatin and cancerK22CA229612 · NCI · WASHINGTON UNIVERSITY · PI SOUROULLAS, GEORGE P. · 2018 to 2020
$504k
NCI NIH HHS K22 CA229612NCI NIH HHS T32 CA113275
6 · The paper itself

Abstract

Mutations in chromatin modifying genes frequently occur in many kinds of cancer. Most mechanistic studies focus on their canonical functions, while therapeutic approaches target their enzymatic activity. Recent studies, however, demonstrate that non-canonical functions of chromatin modifiers may be equally important and therapeutically actionable in different types of cancer. One epigenetic regulator that demonstrates such a dual role in cancer is the histone methyltransferase EZH2. EZH2 is a core component of the polycomb repressive complex 2 (PRC2), which plays a crucial role in cell identity, differentiation, proliferation, stemness and plasticity. While much of the regulatory functions and oncogenic activity of EZH2 have been attributed to its canonical, enzymatic activity of methylating lysine 27 on histone 3 (H3K27me3), a repressive chromatin mark, recent studies suggest that non-canonical functions that are independent of H3K27me3 also contribute towards the oncogenic activity of EZH2. Contrary to PRC2's canonical repressive activity, mediated by H3K27me3, outside of the complex EZH2 can directly interact with transcription factors and oncogenes to activate gene expression. A more focused investigation into these non-canonical interactions of EZH2 and other epigenetic/chromatin regulators may uncover new and more effective therapeutic strategies. Here, we summarize major findings on the non-canonical functions of EZH2 and how they are related to different aspects of carcinogenesis.

Indexed as

cancerEZH2H3K27me3non-canonicaloncogenetumor suppressor

Identifiers

PMID37664059
PMCPMC10473085
OpenAlexW4385977848

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.