Evidence map›Paper›PMID 28150704›Full record

ArticleScientific reports2017

Genome-wide DNA methylation reprogramming in response to inorganic arsenic links inhibition of CTCF binding, DNMT expression and cellular transformation.

Matthew Rea, Meredith Eckstein, Rebekah Eleazer, Caroline Smith, Yvonne N Fondufe-Mittendorf

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Single-Base Methylome Analysis of Sweet Cherry (International journal of molecular sciences · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Epigenomic reprogramming in iAs-mediated carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Chronic Exposure to Cadmium Induces Differential Methylation in Mice Spermatozoa.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Matthew ReaDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY 40536, USA.
Meredith EcksteinDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY 40536, USA.
Rebekah EleazerDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY 40536, USA.
Caroline SmithDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY 40536, USA.
Yvonne N Fondufe-MittendorfDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY 40536, USA.
University of Kentucky · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers · 2013 to 2026
$38.3M
Interdisciplinary Research Training in Cancer BiologyT32CA165990 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers, KATHLEEN L. O'CONNOR · 2013 to 2026
$3.2M
The role of chromatin structural and epigenetic changes in arsenic-induced gene expressionR01ES024478 · NIEHS · UNIVERSITY OF KENTUCKY · PI FONDUFE-MITTENDORF, YVONNE NSOKIKA · 2015 to 2019
$1.8M
NCI NIH HHS P30 CA177558NCI NIH HHS T32 CA165990NIEHS NIH HHS R01 ES024478
6 · The paper itself

Abstract

Chronic low dose inorganic arsenic (iAs) exposure leads to changes in gene expression and epithelial-to-mesenchymal transformation. During this transformation, cells adopt a fibroblast-like phenotype accompanied by profound gene expression changes. While many mechanisms have been implicated in this transformation, studies that focus on the role of epigenetic alterations in this process are just emerging. DNA methylation controls gene expression in physiologic and pathologic states. Several studies show alterations in DNA methylation patterns in iAs-mediated pathogenesis, but these studies focused on single genes. We present a comprehensive genome-wide DNA methylation analysis using methyl-sequencing to measure changes between normal and iAs-transformed cells. Additionally, these differential methylation changes correlated positively with changes in gene expression and alternative splicing. Interestingly, most of these differentially methylated genes function in cell adhesion and communication pathways. To gain insight into how genomic DNA methylation patterns are regulated during iAs-mediated carcinogenesis, we show that iAs probably targets CTCF binding at the promoter of DNA methyltransferases, regulating their expression. These findings reveal how CTCF binding regulates DNA methyltransferase to reprogram the methylome in response to an environmental toxin.

Indexed as

Genome, HumanAlternative SplicingArsenicCCCTC-Binding FactorCell Transformation, NeoplasticCellular ReprogrammingChromosomes, HumanCpG IslandsDNA (Cytosine-5-)-MethyltransferasesDNA MethylationEpithelial-Mesenchymal TransitionGene OntologyHumansPromoter Regions, GeneticProtein BindingReproducibility of ResultsArsenicCCCTC-Binding FactorDNA (Cytosine-5-)-Methyltransferases

Identifiers

PMID28150704
PMCPMC5288714
OpenAlexW2584776413

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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.