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

Overview of attention for article published in BMC Cancer, February 2016
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (85th percentile)
  • High Attention Score compared to outputs of the same age and source (92nd percentile)

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Title
The dual specificity phosphatase 2 gene is hypermethylated in human cancer and regulated by epigenetic mechanisms
Published in
BMC Cancer, February 2016
DOI 10.1186/s12885-016-2087-6
Pubmed ID
Authors

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

Abstract

Dual 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. We 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. Here 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. Our data show that aberrant epigenetic inactivation of DUSP2 occurs in carcinogenesis and that CTCF is involved in the epigenetic regulation of DUSP2 expression.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 29 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 29 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 21%
Student > Bachelor 5 17%
Student > Master 3 10%
Researcher 3 10%
Student > Doctoral Student 2 7%
Other 1 3%
Unknown 9 31%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 17%
Medicine and Dentistry 4 14%
Agricultural and Biological Sciences 2 7%
Immunology and Microbiology 2 7%
Chemistry 2 7%
Other 5 17%
Unknown 9 31%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 10. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 13 December 2022.
All research outputs
#3,154,977
of 23,323,574 outputs
Outputs from BMC Cancer
#706
of 8,445 outputs
Outputs of similar age
#57,766
of 399,809 outputs
Outputs of similar age from BMC Cancer
#16
of 200 outputs
Altmetric has tracked 23,323,574 research outputs across all sources so far. Compared to these this one has done well and is in the 86th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 8,445 research outputs from this source. They receive a mean Attention Score of 4.4. This one has done particularly well, scoring higher than 91% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 399,809 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 85% of its contemporaries.
We're also able to compare this research output to 200 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 92% of its contemporaries.