Evidence map›Paper›PMID 33514701›Full record

ArticleNature communications2021

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands.

Roza H Ali Masalmeh, Francesca Taglini, Cristina Rubio-Ramon, Kamila I Musialik, Jonathan Higham, Hazel Davidson-Smith, Ioannis Kafetzopoulos, Kamila P Pawlicka, Hannah M Finan, Richard Clark and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  6. T-Cadherin (International journal of molecular sciences · 2025
    Review
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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

14 authors at 4 institutions in 1 country.

Roza H Ali MasalmehMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK.
Francesca TagliniMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK.
Cristina Rubio-RamonMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK.
Kamila I MusialikMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK.
Jonathan HighamMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK.
Hazel Davidson-SmithMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK.
Ioannis KafetzopoulosMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK.ORCID 0000-0001-5948-3455
Kamila P PawlickaMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK.
Hannah M FinanMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK.
Richard ClarkEdinburgh Clinical Research Facility, University of Edinburgh, Edinburgh, UK.ORCID 0000-0002-0066-1541
Jimi WillsCRUK Edinburgh Centre, IGMM, University of Edinburgh, Edinburgh, UK.
Andrew J FinchCRUK Edinburgh Centre, IGMM, University of Edinburgh, Edinburgh, UK.
Lee MurphyEdinburgh Clinical Research Facility, University of Edinburgh, Edinburgh, UK.ORCID 0000-0001-6467-7449
Duncan SproulMRC Human Genetics Unit, IGMM, University of Edinburgh, Edinburgh, UK. Duncan.Sproul@igmm.ed.ac.uk.ORCID 0000-0001-6168-4563
Edinburgh Cancer Research · GBInstitute of Genetics and Cancer · GBUniversity of Edinburgh · GBQueen Mary University of London · GB

Funding

Cancer Research UK 20837Cancer Research UK C47648/A20837Medical Research Council
6 · The paper itself

Abstract

The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.

Indexed as

DNA MethylationGene Expression Regulation, NeoplasticCarcinogenesisCell Line, TumorChromatin Immunoprecipitation SequencingColonColorectal NeoplasmsCpG IslandsDatasets as TopicDNA (Cytosine-5-)-MethyltransferasesEpigenesis, GeneticGene Knockout TechniquesHistone CodeHistonesHumansPromoter Regions, GeneticDNA (Cytosine-5-)-MethyltransferasesHistones

Identifiers

PMID33514701
PMCPMC7846778
OpenAlexW3123946195

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.