Evidence map›Paper›PMID 27534853›Full record

ArticleBMC medical genomics2016

Frequent hypermethylation of orphan CpG islands with enhancer activity in cancer.

Min Gyun Bae, Jeong Yeon Kim, Jung Kyoon Choi

Abstract read
In one paragraph

Article in BMC medical genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  12. Differential Methylation inInternational journal of molecular sciences · 2019
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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.

Min Gyun BaeDepartment of Bio and Brain Engineering, KAIST, Daejeon, 305-701, Republic of Korea.
Jeong Yeon KimDepartment of Bio and Brain Engineering, KAIST, Daejeon, 305-701, Republic of Korea.
Jung Kyoon ChoiDepartment of Bio and Brain Engineering, KAIST, Daejeon, 305-701, Republic of Korea. jungkyoon@kaist.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCpG islands (CGIs) are interspersed DNA sequences that have unusually high CpG ratios and GC contents. CGIs are typically located in the promoter of protein-coding genes. They normally lack DNA methylation but become hypermethylated and induce repression of associated genes in cancer. However, the biological functions of non-promoter CGIs (orphan CGIs) largely remain unclear.

resultsHere, we identify orphan CGIs that do not map to the promoter of any protein-coding or non-coding transcripts but possess chromatin and transcriptional marks that reflect enhancer activity (termed eCGIs). They exhibit three-dimensional chromatin looping toward multiple target genes with high affinity. Intriguingly, transcription regulators were frequently associated with such CGI-containing enhancers. Remarkably, our analyses in cell lines and clinical tissues showed that eCGIs have more dynamic DNA methylation changes in cancer relative to promoter CGIs. The observed eCGI hypermethylation was accompanied by a loss of enhancer marks and transcriptional inactivation of the target genes.

conclusionOur results suggest that eCGIs may constitute a distinct class of enhancers and perform a more instrumental role in tumorigenesis than typical CGIs in gene promoters.

Indexed as

DNA MethylationCell Line, TumorCpG IslandsEnhancer Elements, GeneticEpigenomicsGene Expression ProfilingHumansTranscription, GeneticCancerCpG islandsDNA methylationEnhancers

Identifiers

PMID27534853
PMCPMC4989897

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Registered trials

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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.