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Cells
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Heterochromatin and Tumorigenesis
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Heterochromatin and Tumorigenesis

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 7230

Special Issue Editor

Dr. Florence Cammas

E-Mail Website
Guest Editor
IRCM, Cancer Research Institute of Montpellier, INSERM, U1194, 34298 Montpellier, France
Interests: chromatin; heterochromatin; cancer; HP1; senescence; transcriptional regulation; retrotransposons
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Heterochromatin, the “dark side” of the genome, has long been considered an inert storage site for useless DNA sequences; however, there is increasing evidence that this chromatin compartment is essential for many nuclear functions, including chromosome segregation, regulation of gene expression and of DNA replication, and repair. Heterochromatin, which is mainly composed of repetitive sequences including retrotransposons, is characterized by a high level of compaction, an enrichment of the histone mark H3K9me3 and of the chromatin associated proteins HP1 (Heterochromatin Protein 1), and an extremely limited level of transcriptional activity. Many studies have shown that changing the equilibrium of the different heterochromatin components has devastating consequences in particular in the development of cancers. Several lines of evidence support the view that heterochromatin could prevent tumor development by promoting cellular senescence and by silencing retrotransposon activity. A better understanding of how heterochromatin is acting in regulating tumor development is an exciting and particularly active field of research.

This Special Issue aims at summarizing the current knowledge regarding the role of heterochromatin in cancer development and how targeting components essential for its establishment and/or maintenance could lead to therapeutic breakthroughs for cancer treatment.

Dr. Florence Cammas
Guest Editor

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 submissions that pass pre-check are 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. Cells is an international peer-reviewed open access semimonthly 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 2700 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.

Keywords

  • heterochromatin
  • cancer
  • nuclear organization
  • transcriptional silencing
  • retrotransposons

Published Papers (3 papers)

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Research

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17 pages, 2522 KiB  
Article
Endogenous Retroviral Sequences Behave as Putative Enhancers Controlling Gene Expression through HP1-Regulated Long-Range Chromatin Interactions
by Sébastien Calvet, Séphora Sallis, Nehmé Saksouk, Cosette Rebouissou, Catherine Teyssier, Annick Lesne, Florence Cammas and Thierry Forné
Cells 2022, 11(15), 2392; https://doi.org/10.3390/cells11152392 - 03 Aug 2022
Viewed by 1867
Abstract
About half of the mammalian genome is constituted of repeated elements, among which endogenous retroviruses (ERVs) are known to influence gene expression and cancer development. The HP1 (Heterochromatin Protein 1) proteins are known to be essential for heterochromatin establishment and function and its [...] Read more.
About half of the mammalian genome is constituted of repeated elements, among which endogenous retroviruses (ERVs) are known to influence gene expression and cancer development. The HP1 (Heterochromatin Protein 1) proteins are known to be essential for heterochromatin establishment and function and its loss in hepatocytes leads to the reactivation of specific ERVs and to liver tumorigenesis. Here, by studying two ERVs located upstream of genes upregulated upon loss of HP1, Mbd1 and Trim24, we show that these HP1-dependent ERVs behave as either alternative promoters or as putative enhancers forming a loop with promoters of endogenous genes depending on the genomic context and HP1 expression level. These ERVs are characterised by a specific HP1-independent enrichment in heterochromatin-associated marks H3K9me3 and H4K20me3 as well as in the enhancer-specific mark H3K4me1, a combination that might represent a bookmark of putative ERV-derived enhancers. These ERVs are further enriched in a HP1-dependent manner in H3K27me3, suggesting a critical role of this mark together with HP1 in the silencing of the ERVs, as well as for the repression of the associated genes. Altogether, these results lead to the identification of a new regulatory hub involving the HP1-dependent formation of a physical loop between specific ERVs and endogenous genes. Full article
(This article belongs to the Special Issue Heterochromatin and Tumorigenesis)
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20 pages, 1161 KiB  
Article
The HPSE Gene Insulator—A Novel Regulatory Element That Affects Heparanase Expression, Stem Cell Mobilization, and the Risk of Acute Graft versus Host Disease
by Olga Ostrovsky, Polina Baryakh, Yan Morgulis, Margarita Mayorov, Nira Bloom, Katia Beider, Avichai Shimoni, Israel Vlodavsky and Arnon Nagler
Cells 2021, 10(10), 2523; https://doi.org/10.3390/cells10102523 - 23 Sep 2021
Cited by 4 | Viewed by 1770
Abstract
The HPSE gene encodes heparanase (HPSE), a key player in cancer, inflammation, and autoimmunity. We have previously identified a strong HPSE gene enhancer involved in self-regulation of heparanase by negative feedback exerted in a functional rs4693608 single-nucleotide polymorphism (SNP) dependent manner. In the [...] Read more.
The HPSE gene encodes heparanase (HPSE), a key player in cancer, inflammation, and autoimmunity. We have previously identified a strong HPSE gene enhancer involved in self-regulation of heparanase by negative feedback exerted in a functional rs4693608 single-nucleotide polymorphism (SNP) dependent manner. In the present study, we analyzed the HPSE gene insulator region, located in intron 9 and containing rs4426765, rs28649799, and rs4364254 SNPs. Our results indicate that this region exhibits HPSE regulatory activity. SNP substitutions lead to modulation of a unique DNA-protein complex that affects insulator activity. Analysis of interactions between enhancer and insulator SNPs revealed that rs4693608 has a major effect on HPSE expression and the risk of post-transplantation acute graft versus host disease (GVHD). The C alleles of insulator SNPs rs4364254 and rs4426765 modify the activity of the HPSE enhancer, resulting in altered HPSE expression and increased risk of acute GVHD. Moreover, rs4426765 correlated with HPSE expression in activated mononuclear cells, as well as with CD3 levels and lymphocyte counts following G-CSF mobilization. rs4363084 and rs28649799 were found to be associated with CD34+ levels. Our study provides new insight into the mechanism of HPSE gene regulation and its impact on normal and pathological processes in the hematopoietic system. Full article
(This article belongs to the Special Issue Heterochromatin and Tumorigenesis)
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Review

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11 pages, 1039 KiB  
Review
Restructuring of Lamina-Associated Domains in Senescence and Cancer
by Aurélie Bellanger, Julia Madsen-Østerbye, Natalia M. Galigniana and Philippe Collas
Cells 2022, 11(11), 1846; https://doi.org/10.3390/cells11111846 - 05 Jun 2022
Cited by 11 | Viewed by 2829
Abstract
Induction of cellular senescence or cancer is associated with a reshaping of the nuclear envelope and a broad reorganization of heterochromatin. At the periphery of mammalian nuclei, heterochromatin is stabilized at the nuclear lamina via lamina-associated domains (LADs). Alterations in the composition of [...] Read more.
Induction of cellular senescence or cancer is associated with a reshaping of the nuclear envelope and a broad reorganization of heterochromatin. At the periphery of mammalian nuclei, heterochromatin is stabilized at the nuclear lamina via lamina-associated domains (LADs). Alterations in the composition of the nuclear lamina during senescence lead to a loss of peripheral heterochromatin, repositioning of LADs, and changes in epigenetic states of LADs. Cancer initiation and progression are also accompanied by a massive reprogramming of the epigenome, particularly in domains coinciding with LADs. Here, we review recent knowledge on alterations in chromatin organization and in the epigenome that affect LADs and related genomic domains in senescence and cancer. Full article
(This article belongs to the Special Issue Heterochromatin and Tumorigenesis)
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