Previous Issue

Table of Contents

Epigenomes, Volume 2, Issue 1 (March 2018)

  • Issues are regarded as officially published after their release is announced to the table of contents alert mailing list.
  • You may sign up for e-mail alerts to receive table of contents of newly released issues.
  • PDF is the official format for papers published in both, html and pdf forms. To view the papers in pdf format, click on the "PDF Full-text" link, and use the free Adobe Readerexternal link to open them.
View options order results:
result details:
Displaying articles 1-5
Export citation of selected articles as:

Editorial

Jump to: Research, Review, Other

Open AccessEditorial Acknowledgement to Reviewers of Epigenomes in 2017
Epigenomes 2018, 2(1), 2; doi:10.3390/epigenomes2010002
Received: 25 January 2018 / Revised: 25 January 2018 / Accepted: 25 January 2018 / Published: 27 January 2018
PDF Full-text (633 KB) | HTML Full-text | XML Full-text
Abstract
Peer review is an essential part in the publication process, ensuring that Epigenomes maintains high quality standards for its published papers. [...]
Full article

Research

Jump to: Editorial, Review, Other

Open AccessArticle Panobinostat Potentiates Temozolomide Effects and Reverses Epithelial–Mesenchymal Transition in Glioblastoma Cells
Epigenomes 2018, 2(1), 5; doi:10.3390/epigenomes2010005
Received: 30 December 2017 / Revised: 6 February 2018 / Accepted: 13 February 2018 / Published: 19 February 2018
PDF Full-text (1612 KB) | HTML Full-text | XML Full-text
Abstract
Glioblastoma is the most common form of glioma, as well as the most aggressive. Patients suffering from this disease have a very poor prognosis. Surgery, radiotherapy, and temozolomide are the only approved treatments nowadays. Panobinostat is a pan-inhibitor of histone deacetylases (HDACs) that
[...] Read more.
Glioblastoma is the most common form of glioma, as well as the most aggressive. Patients suffering from this disease have a very poor prognosis. Surgery, radiotherapy, and temozolomide are the only approved treatments nowadays. Panobinostat is a pan-inhibitor of histone deacetylases (HDACs) that has been shown to break some pathways which play an important role in cancer development. A global intention of using panobinostat as a therapeutic agent against glioblastoma is beginning to be a reality. We have treated the LN405 glioblastoma cell line with temozolomide, panobinostat, and combined treatment, in order to test apoptosis, colony formation, and a possible molecular reversion of the mesenchymal phenotype of the cells to an epithelial one. Our results show that panobinostat decreased N-cadherin levels in the LN405 glioblastoma cell line while it increased the expression of E-cadherin, which might be associated with a mesenchymal–epithelial transition in glioblastoma cells. Colony formation was reduced, and apoptosis was increased with treatments. Our research highlights the importance of panobinostat as a potential adjuvant therapy to be used with temozolomide to treat glioblastoma and the advantages of the combined treatment versus temozolomide alone, which is currently the first-line treatment used to treat this tumor. Full article
Figures

Figure 1

Review

Jump to: Editorial, Research, Other

Open AccessReview Drosophila DNA-Binding Proteins in Polycomb Repression
Epigenomes 2018, 2(1), 1; doi:10.3390/epigenomes2010001
Received: 5 November 2017 / Revised: 10 January 2018 / Accepted: 10 January 2018 / Published: 16 January 2018
PDF Full-text (8141 KB) | HTML Full-text | XML Full-text
Abstract
The formation of individual gene expression patterns in different cell types is required during differentiation and development of multicellular organisms. Polycomb group (PcG) proteins are key epigenetic regulators responsible for gene repression, and dysregulation of their activities leads to developmental abnormalities and diseases.
[...] Read more.
The formation of individual gene expression patterns in different cell types is required during differentiation and development of multicellular organisms. Polycomb group (PcG) proteins are key epigenetic regulators responsible for gene repression, and dysregulation of their activities leads to developmental abnormalities and diseases. PcG proteins were first identified in Drosophila, which still remains the most convenient system for studying PcG-dependent repression. In the Drosophila genome, these proteins bind to DNA regions called Polycomb response elements (PREs). A major role in the recruitment of PcG proteins to PREs is played by DNA-binding factors, several of which have been characterized in detail. However, current knowledge is insufficient for comprehensively describing the mechanism of this process. In this review, we summarize and discuss the available data on the role of DNA-binding proteins in PcG recruitment to chromatin. Full article
(This article belongs to the Special Issue Polycomb and Trithorax Group of Proteins in Development and Disease)
Figures

Figure 1

Open AccessReview From Flies to Mice: The Emerging Role of Non-Canonical PRC1 Members in Mammalian Development
Epigenomes 2018, 2(1), 4; doi:10.3390/epigenomes2010004
Received: 9 November 2017 / Revised: 19 December 2017 / Accepted: 22 January 2018 / Published: 5 February 2018
PDF Full-text (3525 KB) | HTML Full-text | XML Full-text
Abstract
Originally two types of Polycomb Repressive Complexes (PRCs) were described, canonical PRC1 (cPRC1) and PRC2. Recently, a versatile set of complexes were identified and brought up several dilemmas in PRC mediated repression. These new class of complexes were named as non-canonical PRC1s (ncPRC1s).
[...] Read more.
Originally two types of Polycomb Repressive Complexes (PRCs) were described, canonical PRC1 (cPRC1) and PRC2. Recently, a versatile set of complexes were identified and brought up several dilemmas in PRC mediated repression. These new class of complexes were named as non-canonical PRC1s (ncPRC1s). Both cPRC1s and ncPRC1s contain Ring finger protein (RING1, RNF2) and Polycomb group ring finger catalytic (PCGF) core, but in ncPRCs, RING and YY1 binding protein (RYBP), or YY1 associated factor 2 (YAF2), replaces the Chromobox (CBX) and Polyhomeotic (PHC) subunits found in cPRC1s. Additionally, ncPRC1 subunits can associate with versatile accessory proteins, which determine their functional specificity. Homozygous null mutations of the ncPRC members in mice are often lethal or cause infertility, which underlines their essential functions in mammalian development. In this review, we summarize the mouse knockout phenotypes of subunits of the six major ncPRCs. We highlight several aspects of their discovery from fly to mice and emerging role in target recognition, embryogenesis and cell-fate decision making. We gathered data from stem cell mediated in vitro differentiation assays and genetically engineered mouse models. Accumulating evidence suggests that ncPRC1s play profound role in mammalian embryogenesis by regulating gene expression during lineage specification of pluripotent stem cells. Full article
(This article belongs to the Special Issue Polycomb and Trithorax Group of Proteins in Development and Disease)
Figures

Figure 1

Other

Jump to: Editorial, Research, Review

Open AccessPerspective 5-Hydroxymethylcytosine (5hmC), or How to Identify Your Favorite Cell
Epigenomes 2018, 2(1), 3; doi:10.3390/epigenomes2010003
Received: 20 December 2017 / Revised: 23 January 2018 / Accepted: 23 January 2018 / Published: 30 January 2018
PDF Full-text (1609 KB) | HTML Full-text | XML Full-text
Abstract
Recently described as the sixth base of the DNA macromolecule, the precise role of 5-hydroxymethylcytosine (5hmC) is the subject of debate. Early studies indicate that it is functionally distinct from cytosine DNA methylation (5mC), and there is evidence for 5hmC being a stable
[...] Read more.
Recently described as the sixth base of the DNA macromolecule, the precise role of 5-hydroxymethylcytosine (5hmC) is the subject of debate. Early studies indicate that it is functionally distinct from cytosine DNA methylation (5mC), and there is evidence for 5hmC being a stable derivate of 5mC, rather than just an intermediate of demethylation. Moreover, 5hmC events correlate in time and space with key differentiation steps in mammalian cells. Such events span the three embryonic germ layers and multiple progenitor cell subtypes, suggesting a general mechanism. Because of the growing understanding of the role of progenitor cells in disease origin, we attempted to provide a detailed summary on the currently available literature supporting 5hmC as a key player in adult progenitor cell differentiation. This summary consolidates the emerging role for 5hmC in defining cellular fate. Full article
Figures

Figure 1

Back to Top