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DNA methylation and histone modifications regulate SOX11 expression in lymphoid and solid cancer cells

Overview of attention for article published in BMC Cancer, April 2015
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Title
DNA methylation and histone modifications regulate SOX11 expression in lymphoid and solid cancer cells
Published in
BMC Cancer, April 2015
DOI 10.1186/s12885-015-1208-y
Pubmed ID
Authors

Lena Nordström, Elin Andersson, Venera Kuci, Elin Gustavsson, Karolina Holm, Markus Ringnér, Per Guldberg, Sara Ek

Abstract

The neural transcription factor SOX11 is present at specific stages during embryo development with a very restricted expression in adult tissue, indicating precise regulation of transcription. SOX11 is strongly up-regulated in some malignancies and have a functional role in tumorgenesis. With the aim to explore differences in epigenetic regulation of SOX11 expression in normal versus neoplastic cells, we investigated methylation and histone modifications related to the SOX11 promoter and the possibility to induce re-expression using histone deacetylase (HDAC) or EZH2 inhibitors. The epigenetic regulation of SOX11 was investigated in distinct non-malignant cell populations (n = 7) and neoplastic cell-lines (n = 42) of different cellular origins. DNA methylation was assessed using bisulfite sequencing, methylation-specific melting curve analysis, MethyLight and pyrosequencing. The presence of H3K27me3 was assessed using ChIP-qPCR. The HDAC inhibitors Vorinostat and trichostatin A were used to induce SOX11 in cell lines with no endogenous expression. The SOX11 promoter shows a low degree of methylation and strong enrichment of H3K27me3 in non-malignant differentiated cells, independent of cellular origin. Cancers of the B-cell lineage are strongly marked by de novo methylation at the SOX11 promoter in SOX11 non-expressing cells, while solid cancer entities display a more varying degree of SOX11 promoter methylation. The silencing mark H3K27me3 was generally present at the SOX11 promoter in non-expressing cells, and an increased enrichment was observed in cancer cells with a low degree of SOX11 methylation compared to cells with dense methylation. Finally, we demonstrate that the HDAC inhibitors (vorinostat and trichostatin A) induce SOX11 expression in cancer cells with low levels of SOX11 methylation. We show that SOX11 is strongly marked by repressive histone marks in non-malignant cells. In contrast, SOX11 regulation in neoplastic tissues is more complex involving both DNA methylation and histone modifications. The possibility to re-express SOX11 in non-methylated tissue is of clinical relevance, and was successfully achieved in cell lines with low levels of SOX11 methylation. In breast cancer patients, methylation of the SOX11 promoter was shown to correlate with estrogen receptor status, suggesting that SOX11 may be functionally re-expressed during treatment with HDAC inhibitors in specific patient subgroups.

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Mendeley readers

The data shown below were compiled from readership statistics for 21 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 21 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 7 33%
Student > Ph. D. Student 4 19%
Student > Master 3 14%
Student > Bachelor 2 10%
Professor 1 5%
Other 3 14%
Unknown 1 5%
Readers by discipline Count As %
Agricultural and Biological Sciences 10 48%
Biochemistry, Genetics and Molecular Biology 7 33%
Computer Science 1 5%
Medicine and Dentistry 1 5%
Unknown 2 10%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 17 April 2015.
All research outputs
#4,184,721
of 5,005,423 outputs
Outputs from BMC Cancer
#2,239
of 2,801 outputs
Outputs of similar age
#140,157
of 169,271 outputs
Outputs of similar age from BMC Cancer
#173
of 199 outputs
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