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Epigenetic and Genetic Instability in Cancer: From Basic Mechanisms to...
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Epigenetic and Genetic Instability in Cancer: From Basic Mechanisms to Translational and Clinical Applications

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (25 November 2023) | Viewed by 2888

Special Issue Editors

Prof. Dr. Rabii Ameziane El Hassani

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Guest Editor
Laboratory of Biology of Human Pathologies ‘BioPatH’, Faculty of Sciences, Mohammed V University in Rabat, Rabat, Morocco
Interests: oxidative stress; NADPH oxidases; epi/genetic instability; cancer; biomarker
Dr. Said Aoufouchi

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Guest Editor
Institut de Cancerologie Gustave Roussy, Villejuif, France
Interests: humoral immunity; immunoglobulin genes; B cell biology; B lymphomagenesis; DNA repair; mutagenesis; TLS polymerases; epigenetic and cell cycle
Special Issues, Collections and Topics in MDPI journals
Dr. Leticia Lerner

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Guest Editor
Institut Jacques Monod CNRS, Université Paris Cité, UMR 7592, Paris, France
Interests: DNA replication; DNA repair; epigenetic stability; cancer metabolism; programmed DNA elimination
Dr. Xavier Renaudin

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Guest Editor
Department of Genome Integrity & Cancers, CNRS-UMR 9019, Institut Gustave Roussy, Villejuif, CEDEX, France
Interests: DNA repair; epigenetic maintenance; transcription; genotoxic stress; oxidative stress; mitochondiral metabolism; fanconi anemia; breast cancer

Special Issue Information

Dear Colleagues,

Cancer, a real worldwide public health problem, is a multifactorial disease sharing both epigenetic and genetic instability. Deciphering molecular mechanisms that could initiate and promote these instabilities is of great interest in the aim to improve our knowledge regarding cellular transformation as well as translational and clinical applications.

Therefore, we are pleased to invite you to contribute to this Special Issue on ‘Epigenetic and Genetic Instability in Cancer: From Basic Mechanisms to Translational and Clinical Applications’.

In this Special Issue, we seek original research, review, mini-review, hypothesis and theory, clinical trial and opinion articles that cover but are not limited to the following subjects:
  • Understanding the molecular mechanisms of epigenetic instability in cancer: DNA methylation, microRNA, histone modifications;
  • Understanding the molecular mechanisms of genetic instability in cancer: DNA damage signaling and DNA repair proteins, oncogenes, tumor suppressors;
  • Spatiotemporal dynamics of chromatin in cancer;
  • Epigenetics and associated mechanisms that alter chromatin in response to physiological or pathological signals;
  • Genome editing technology in cancer;
  • Methods of detection/analysis of genetic and epigenetic instability in cancer;
  • Genetic and epigenetic biomarkers: identification approaches and clinical use.

Prof. Dr. Rabii Ameziane El Hassani
Dr. Said Aoufouchi
Dr. Leticia Lerner
Dr. Xavier Renaudin
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 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. Genes is an international peer-reviewed open access monthly 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 2600 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

  • cancer
  • (epi)genetic instability
  • DNA repair
  • chromatin remodeling
  • (epi)mutations
  • (epi)genome editing
  • diagnostic and prognostic biomarkers
  • chromatin-modifying enzymes

Published Papers (2 papers)

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Research

15 pages, 2265 KiB  
Article
Biomarker RIPK3 Is Silenced by Hypermethylation in Melanoma and Epigenetic Editing Reestablishes Its Tumor Suppressor Function
by Sarah Arroyo Villora, Paula Castellanos Silva, Tamara Zenz, Ji Sun Kwon, Nico Schlaudraff, Dafina Nitaj, Cornelia Meckbach, Reinhard Dammann and Antje M. Richter
Genes 2024, 15(2), 175; https://doi.org/10.3390/genes15020175 - 28 Jan 2024
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Abstract
For several decades, cancers have demonstrably been one of the most frequent causes of death worldwide. In addition to genetic causes, cancer can also be caused by epigenetic gene modifications. Frequently, tumor suppressor genes are epigenetically inactivated due to hypermethylation of their CpG [...] Read more.
For several decades, cancers have demonstrably been one of the most frequent causes of death worldwide. In addition to genetic causes, cancer can also be caused by epigenetic gene modifications. Frequently, tumor suppressor genes are epigenetically inactivated due to hypermethylation of their CpG islands, actively contributing to tumorigenesis. Since CpG islands are usually localized near promoters, hypermethylation of the promoter can have a major impact on gene expression. In this study, the potential tumor suppressor gene Receptor Interacting Serine/Threonine Protein Kinase 3 (RIPK3) was examined for an epigenetic regulation and its gene inactivation in melanomas. A hypermethylation of the RIPK3 CpG island was detected by bisulfite pyrosequencing and was accompanied by a correlated loss of its expression. In addition, an increasing RIPK3 methylation rate was observed with increasing tumor stage of melanomas. For further epigenetic characterization of RIPK3, epigenetic modulation was performed using a modified CRISPR/dCas9 (CRISPRa activation) system targeting its DNA hypermethylation. We observed a reduced fitness of melanoma cells by (re-)expression and demethylation of the RIPK3 gene using the epigenetic editing-based method. The tumor suppressive function of RIPK3 was evident by phenotypic determination using fluorescence microscopy, flow cytometry and wound healing assay. Our data highlight the function of RIPK3 as an epigenetically regulated tumor suppressor in melanoma, allowing it to be classified as a biomarker. Full article
(This article belongs to the Special Issue Epigenetic and Genetic Instability in Cancer: From Basic Mechanisms to Translational and Clinical Applications)
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15 pages, 1660 KiB  
Article
BRCA1 Promoter Hypermethylation in Malignant Breast Tumors and in the Histologically Normal Adjacent Tissues to the Tumors: Exploring Its Potential as a Biomarker and Its Clinical Significance in a Translational Approach
by Yassire Oubaddou, Mohamed Oukabli, Salma Fenniche, Abderrahim Elktaibi, Mohamed Reda Elochi, Abderrahmane Al Bouzidi, Zineb Qmichou, Nadia Dakka, Caroline Diorio, Antje Richter, Youssef Bakri and Rabii Ameziane El Hassani
Genes 2023, 14(9), 1680; https://doi.org/10.3390/genes14091680 - 25 Aug 2023
Cited by 1 | Viewed by 1470
Abstract
The hypermethylation status of the promoter region of the breast cancer 1 (BRCA1), a well-known tumor suppressor gene, has been extensively investigated in the last two decades as a potential biomarker for breast cancer. In this retrospective study, we investigated the [...] Read more.
The hypermethylation status of the promoter region of the breast cancer 1 (BRCA1), a well-known tumor suppressor gene, has been extensively investigated in the last two decades as a potential biomarker for breast cancer. In this retrospective study, we investigated the prevalence of BRCA1 promoter methylation in 84 human breast tissues, and we correlated this epigenetic silencing with the clinical and histopathological parameters of breast cancer. We used methylation-specific PCR (MSP) to analyze BRCA1 promoter hypermethylation in 48 malignant breast tumors (MBTs), 15 normal adjacent tissues (NATs), and 21 benign breast lesions (BBLs). The results showed that BRCA1 promoter hypermethylation was higher in MBTs (20/48; 41.67%) and NATs (7/15; 46.67%) compared to BBLs (4/21; 19.05%). The high percentage of BRCA1 hypermethylation in the histologically normal adjacent tissues to the tumors (NATs) suggests the involvement of this epigenetic silencing as a potential biomarker of the early genomic instability in NATs surrounding the tumors. The detection of BRCA1 promoter hypermethylation in BBLs reinforces this suggestion, knowing that a non-negligible rate of benign breast lesions was reported to evolve into cancer. Moreover, our results indicated that the BRCA1 promoter hypermethylated group of MBTs exhibited higher rates of aggressive features, as indicated by the SBR III grade (14/19; 73.68%), elevated Ki67 levels (13/16; 81.25%), and Her2 receptor overexpression (5/20; 25%). Finally, we observed a concordance (60%) in BRCA1 promoter hypermethylation status between malignant breast tumors and their paired histologically normal adjacent tissues. This study highlights the role of BRCA1 promoter hypermethylation as a potential useful biomarker of aggressiveness in MBTs and as an early marker of genomic instability in both histological NATs and BBLs. Full article
(This article belongs to the Special Issue Epigenetic and Genetic Instability in Cancer: From Basic Mechanisms to Translational and Clinical Applications)
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