Special Issue "Biological Methylation in Development and Cancer 2.0"

A special issue of Epigenomes (ISSN 2075-4655).

Deadline for manuscript submissions: closed (31 July 2019).

Special Issue Editors

Dr. Gaetano Verde
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Guest Editor
Department of Basic Sciences, Faculty of Medicine and Health Sciences, Universidad Internacional de Cataluña (UIC), Carrer de Josep Trueta, 08195 Sant Cugat del Vallès, Barcelona, Spain
Interests: epigenetics; gene expression; DNA methylation; cancer; genetic diseases
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Ernesto Guccione
E-Mail Website
Guest Editor
Icahn School of Medicine at Mount Sinai, Hess Center for Science and Medicine, New York, NY, USA
Interests: methyltransferases; transcription; splicing; cancer; genomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the past few years, epigenetic studies have changed the way we see cell reprogramming and differentiation. Now we know that there is no need for the existence of a DNA mutation to change the fate of a cell, and that epigenetic changes at the chromatin level can be sufficient. Of all the possible epigenetic modifications, Methylation has historically been considered one of the most stable. This view, however, has changed radically with the discovery of mechanisms that allow the removal of methyl marks from DNA, RNA, and proteins.

Importantly, while DNA methyltransferases inhibitors have long been tested in patients, more recently protein methyltransferases have also proven to be druggable enzymes, and selective and potent inhibitors have recently entered clinical trials, with great promise for targeted cancer therapy.

This Special Issue will be focused around epigenetic changes conducted by methyltransferases and demethylases and how these changes at the DNA or protein level regulate normal development or lead to cancerous transformation. We will consider research or methods manuscripts of exceptional interest on the following topics:

  • The effect of methyltransferases and demethylases implicated in the development of any model organism;
  • The effect of methyltransferases and demethylases implicated in cancer;
  • The development of novel small molecule inhibitors of methyltransferases and demethylases;
  • Clinical studies investigating the role of methyltransferases and demethylases in cancer.

Dr. Ernesto Guccione
Dr. Gaetano Verde
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Epigenomes is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (1 paper)

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Review

Review
Epigenetic Regulation of EMT (Epithelial to Mesenchymal Transition) and Tumor Aggressiveness: A View on Paradoxical Roles of KDM6B and EZH2
Epigenomes 2019, 3(1), 1; https://0-doi-org.brum.beds.ac.uk/10.3390/epigenomes3010001 - 20 Dec 2018
Cited by 4 | Viewed by 2286
Abstract
EMT (epithelial to mesenchymal transition) is a plastic phenomenon involved in metastasis formation. Its plasticity is conferred in a great part by its epigenetic regulation. It has been reported that the trimethylation of lysine 27 histone H3 (H3K27me3) was a master regulator of [...] Read more.
EMT (epithelial to mesenchymal transition) is a plastic phenomenon involved in metastasis formation. Its plasticity is conferred in a great part by its epigenetic regulation. It has been reported that the trimethylation of lysine 27 histone H3 (H3K27me3) was a master regulator of EMT through two antagonist enzymes that regulate this mark, the methyltransferase EZH2 (enhancer of zeste homolog 2) and the lysine demethylase KDM6B (lysine femethylase 6B). Here we report that EZH2 and KDM6B are overexpressed in numerous cancers and involved in the aggressive phenotype and EMT in various cell lines by regulating a specific subset of genes. The first paradoxical role of these enzymes is that they are antagonistic, but both involved in cancer aggressiveness and EMT. The second paradoxical role of EZH2 and KDM6B during EMT and cancer aggressiveness is that they are also inactivated or under-expressed in some cancer types and linked to epithelial phenotypes in other cancer cell lines. We also report that new cancer therapeutic strategies are targeting KDM6B and EZH2, but the specificity of these treatments may be increased by learning more about the mechanisms of action of these enzymes and their specific partners or target genes in different cancer types. Full article
(This article belongs to the Special Issue Biological Methylation in Development and Cancer 2.0)
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