Evidence map›Paper›PMID 41103952›Full record

ReviewFrontiers in oncology2025

Super-enhancer DNA methylation in cancer: the mechanism of action and therapeutic directions.

Yue Bi, Kang Zou, Ke Wang

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Yue BiDepartment of Orthopedic Oncology, Yantaishan Hospital, Yantai, Shandong, China.
Kang ZouDepartment of Orthopedic Oncology, Yantaishan Hospital, Yantai, Shandong, China.
Ke WangDepartment of Orthopedic Oncology, Yantaishan Hospital, Yantai, Shandong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interplay between DNA methylation and super-enhancer activity is emerging as a key focus in cancer research. Super-enhancers, a specialized class of enhancers, strongly activate transcription of their target genes due to their dense clustering with essential transcription factors (TFs) and cofactors. In cancer, especially, these super-enhancers control key oncogenic drivers and often display abnormal DNA methylation patterns that can repress or overexpress target genes in both solid and blood cancers. Furthermore, DNA methylation in the super-enhancer region has been found to influence their regulatory capacity. Although enhancers are typically characterized by low DNA methylation, dysregulated methylation at super-enhancers is seen in most malignancies, affecting TF and chromatin regulator recruitment. Hypomethylation at these sites often accompanies oncogene hyperactivation, while hypermethylation can repress tumor suppressor mechanisms. Recent research highlights DNA methylation as a promising source of cancer biomarkers. This review examines the intricate relationship between DNA methylation and super-enhancer activity in cancer, concentrating on how methylation regulates super-enhancers, modulates oncogene expression, promotes oncogenesis, and serves as a target for novel oncology therapies.

Indexed as

biomarkercancerDNA methylationmetastasissuper-enhancertumor immunity

Identifiers

PMID41103952
PMCPMC12520912

What OpenQuestion holds

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LicenceCC BY
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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.