Evidence map›Paper›PMID 26833217›Full record

ArticleBMC cancer2016

The dual specificity phosphatase 2 gene is hypermethylated in human cancer and regulated by epigenetic mechanisms.

Tanja Haag, Antje M Richter, Martin B Schneider, Adriana P Jiménez, Reinhard H Dammann

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Article
  11. Expression of Dual-Specificity Phosphatase 2 (DUSP2) in Patients with Serous Ovarian Carcinoma and in SKOV3 and OVCAR3 Cells In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  12. Review
  13. Annals of translational medicine · 2018
    Article
  14. Article
  15. MGMT promoter methylation status in Merkel cell carcinoma: in vitro versus invivo.Journal of cancer research and clinical oncology · 2017
    Article
  16. Article
  17. Article
  18. 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.

Tanja HaagInstitute for Genetics, Justus-Liebig-University, Heinrich-Buff-Ring 58-62, D-35392, Giessen, Germany. Tanjahaag2408@gmail.com.
Antje M RichterInstitute for Genetics, Justus-Liebig-University, Heinrich-Buff-Ring 58-62, D-35392, Giessen, Germany. Antje.M.Richter@gen.bio.uni-giessen.de.
Martin B SchneiderInstitute for Genetics, Justus-Liebig-University, Heinrich-Buff-Ring 58-62, D-35392, Giessen, Germany. Martin.bernd.schneider@onlinehome.de.
Adriana P JiménezInstitute for Genetics, Justus-Liebig-University, Heinrich-Buff-Ring 58-62, D-35392, Giessen, Germany. Adriana.Jimenez@gen.bio.uni-giessen.de.
Reinhard H DammannInstitute for Genetics, Justus-Liebig-University, Heinrich-Buff-Ring 58-62, D-35392, Giessen, Germany. reinhard.dammann@gen.bio.uni-giessen.de.
University of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDual specificity phosphatases are a class of tumor-associated proteins involved in the negative regulation of the MAP kinase pathway. Downregulation of the dual specificity phosphatase 2 (DUSP2) has been reported in cancer. Epigenetic silencing of tumor suppressor genes by abnormal promoter methylation is a frequent mechanism in oncogenesis. It has been shown that the epigenetic factor CTCF is involved in the regulation of tumor suppressor genes.

methodsWe analyzed the promoter hypermethylation of DUSP2 in human cancer, including primary Merkel cell carcinoma by bisulfite restriction analysis and pyrosequencing. Moreover we analyzed the impact of a DNA methyltransferase inhibitor (5-Aza-dC) and CTCF on the epigenetic regulation of DUSP2 by qRT-PCR, promoter assay, chromatin immuno-precipitation and methylation analysis.

resultsHere we report a significant tumor-specific hypermethylation of DUSP2 in primary Merkel cell carcinoma (p = 0.05). An increase in methylation of DUSP2 was also found in 17 out of 24 (71%) cancer cell lines, including skin and lung cancer. Treatment of cancer cells with 5-Aza-dC induced DUSP2 expression by its promoter demethylation, Additionally we observed that CTCF induces DUSP2 expression in cell lines that exhibit silencing of DUSP2. This reactivation was accompanied by increased CTCF binding and demethylation of the DUSP2 promoter.

conclusionsOur data show that aberrant epigenetic inactivation of DUSP2 occurs in carcinogenesis and that CTCF is involved in the epigenetic regulation of DUSP2 expression.

Indexed as

Epigenesis, GeneticCarcinoma, Merkel CellCCCTC-Binding FactorCell Line, TumorCpG IslandsDNA MethylationDual Specificity Phosphatase 2FemaleGene Expression Regulation, NeoplasticHigh-Throughput Nucleotide SequencingHumansMalePromoter Regions, GeneticRepressor ProteinsCCCTC-Binding FactorCTCF protein, humanDual Specificity Phosphatase 2DUSP2 protein, humanRepressor Proteins

Identifiers

PMID26833217
PMCPMC4736155
OpenAlexW2264367776

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.