Pre-neoplastic epigenetic disruption of transcriptional enhancers in chronic inflammation

Aline C. Planello; Rajat Singhania; Ken J. Kron; Swneke D. Bailey; David Roulois; Mathieu Lupien; Sérgio R. Peres Line; Ana Paula de Souza; Daniel D. De Carvalho

doi:10.18632/oncotarget.7513

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

Research Papers:

Pre-neoplastic epigenetic disruption of transcriptional enhancers in chronic inflammation

Aline C. Planello, Rajat Singhania, Ken J. Kron, Swneke D. Bailey, David Roulois, Mathieu Lupien, Sérgio R. Peres Line, Ana Paula de Souza and Daniel D. De Carvalho _

PDF | HTML | Supplementary Files | How to cite

Oncotarget. 2016; 7:15772-15786. https://doi.org/10.18632/oncotarget.7513

Metrics: PDF 2344 views | HTML 2309 views | ?

Abstract

Aline C. Planello1,2,*, Rajat Singhania1,*, Ken J. Kron1, Swneke D. Bailey1, David Roulois1, Mathieu Lupien1,3, Sérgio R. Peres Line2, Ana Paula de Souza2 and Daniel D. De Carvalho1,3

1 Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada

2 Department of Morphology, Piracicaba Dental School, University of Campinas, Piracicaba, SP, Brazil

3 Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada

* These authors have contributed equally to this work

Correspondence to:

Daniel D. De Carvalho, email:

Ana Paula de Souza, email:

Keywords: DNA methylation, enhancers, chronic periodontitis, oral cavity squamous cell carcinoma

Received: December 14, 2015 Accepted: February 09, 2016 Published: February 19, 2016

Abstract

Chronic periodontitis (CP) is a chronic inflammatory disease independently associated with higher incidence of oral cavity squamous cell carcinoma (OSCC). However, the molecular mechanism responsible for this increased incidence is unknown. Here we profiled the DNA methylome of CP patients and healthy controls and compared to a large set of OSCC samples from TCGA. We observed a significant overlap between the altered DNA methylation patterns in CP and in OSCC, suggesting an emergence of a pre-neoplastic epigenome in CP. Remarkably, the hypermethylated CpGs in CP were significantly enriched for enhancer elements. This aberrant enhancer methylation is functional and able to disrupt enhancer activity by preventing the binding of chromatin looping factors. This study provides new insights on the molecular mechanisms linking chronic inflammation and tumor predisposition, highlighting the role of epigenetic disruption of transcriptional enhancers.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 7513

Publication Alerts

Research Papers:

Pre-neoplastic epigenetic disruption of transcriptional enhancers in chronic inflammation

Abstract