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Epigenomes
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New Insights into Epigenetic Regulation in Cancer
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New Insights into Epigenetic Regulation in Cancer

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 2872

Special Issue Editor

Dr. Jason S. Lee

E-Mail Website
Guest Editor
Epigenetics and Disease Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD 4006, Australia
Interests: molecular epigenetics; chromatin dynamics; regulation of gene expression; transcriptomics; hypoxic signalling; cancer metastasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epigenetic modifications of histones as well as DNA and RNA molecules are key regulatory mechanisms that alter gene expression. The deregulation of this process has been recognized as a key factor contributing to tumor development and progression. Epigenetic regulators can silence the expression of tumor suppressors and activate oncogenes, thereby influencing both the initiation and the progression of the disease. In addition, their ability to alter the genetic landscape in response to external stimuli represents a key factor in cellular adaptation to changes in the microenvironment. A molecular understanding of the role that epigenetic regulators play will translate into approaches that advance therapeutic strategies for cancer patients.

The present Special Issue aims to publish high-quality research articles, as well as review contributions, on a variety of topics related to epigenetic regulators and therapeutic developments.

Potential topics include, but are not limited to, the following:

  • Novel epigenetic targets in cancer.
  • Tumor microenvironment.
  • Epitranscriptomics.
  • Epigenetic editing.
  • Current state of epigenetic therapies in cancer.
  • Methods of new epigenetic therapy development.

Dr. Jason S. Lee
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. 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 1500 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 epigenetics
  • epitranscriptomics
  • epigenetic therapy

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Published Papers (3 papers)

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Research

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28 pages, 5546 KiB  
Article
Genome-Wide Methylation Profiling of Peripheral T–Cell Lymphomas Identifies TRIP13 as a Critical Driver of Tumor Proliferation and Survival
by Pawel Nowialis, Julian Tobon, Katarina Lopusna, Jana Opavska, Arshee Badar, Duo Chen, Reem Abdelghany, Gene Pozas, Jacob Fingeret, Emma Noel, Alberto Riva, Hiroshi Fujiwara, Alexander Ishov and Rene Opavsky
Epigenomes 2024, 8(3), 32; https://doi.org/10.3390/epigenomes8030032 - 21 Aug 2024
Viewed by 398
Abstract
Cytosine methylation contributes to the regulation of gene expression and normal hematopoiesis in mammals. It is catalyzed by the family of DNA methyltransferases that include DNMT1, DNMT3A, and DNMT3B. Peripheral T–cell lymphomas (PTCLs) represent aggressive mature T–cell malignancies exhibiting a broad spectrum of [...] Read more.
Cytosine methylation contributes to the regulation of gene expression and normal hematopoiesis in mammals. It is catalyzed by the family of DNA methyltransferases that include DNMT1, DNMT3A, and DNMT3B. Peripheral T–cell lymphomas (PTCLs) represent aggressive mature T–cell malignancies exhibiting a broad spectrum of clinical features with poor prognosis and inadequately understood molecular pathobiology. To better understand the molecular landscape and identify candidate genes involved in disease maintenance, we profiled DNA methylation and gene expression of PTCLs. We found that the methylation patterns in PTCLs are deregulated and heterogeneous but share 767 hypo- and 567 hypermethylated differentially methylated regions (DMRs) along with 231 genes up- and 91 genes downregulated in all samples, suggesting a potential association with tumor development. We further identified 39 hypomethylated promoters associated with increased gene expression in the majority of PTCLs. This putative oncogenic signature included the TRIP13 (thyroid hormone receptor interactor 13) gene whose genetic and pharmacologic inactivation inhibited the proliferation of T–cell lines by inducing G2-M arrest and apoptosis. Our data thus show that human PTCLs have a significant number of recurrent methylation alterations that may affect the expression of genes critical for proliferation whose targeting might be beneficial in anti-lymphoma treatments. Full article
(This article belongs to the Special Issue New Insights into Epigenetic Regulation in Cancer)
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15 pages, 4347 KiB  
Article
DNA Hypomethylation Underlies Epigenetic Swapping between AGO1 and AGO1-V2 Isoforms in Tumors
by Jean S. Fain, Camille Wangermez, Axelle Loriot, Claudia Denoue and Charles De Smet
Epigenomes 2024, 8(3), 24; https://doi.org/10.3390/epigenomes8030024 - 22 Jun 2024
Viewed by 993
Abstract
Human tumors progress in part by accumulating epigenetic alterations, which include gains and losses of DNA methylation in different parts of the cancer cell genome. Recent work has revealed a link between these two opposite alterations by showing that DNA hypomethylation in tumors [...] Read more.
Human tumors progress in part by accumulating epigenetic alterations, which include gains and losses of DNA methylation in different parts of the cancer cell genome. Recent work has revealed a link between these two opposite alterations by showing that DNA hypomethylation in tumors can induce the expression of transcripts that overlap downstream gene promoters and thereby induce their hypermethylation. Preliminary in silico evidence prompted us to investigate if this mechanism applies to the locus harboring AGO1, a gene that plays a central role in miRNA biogenesis and RNA interference. Inspection of public RNA-Seq datasets and RT-qPCR experiments show that an alternative transcript starting 13.4 kb upstream of AGO1 (AGO1-V2) is expressed specifically in testicular germ cells, and becomes aberrantly activated in different types of tumors, particularly in tumors of the esophagus, stomach, and lung. This expression pattern classifies AGO1-V2 into the group of “Cancer-Germline” (CG) genes. Analysis of transcriptomic and methylomic datasets provided evidence that transcriptional activation of AGO1-V2 depends on DNA demethylation of its promoter region. Western blot experiments revealed that AGO1-V2 encodes a shortened isoform of AGO1, corresponding to a truncation of 75 aa in the N-terminal domain, and which we therefore referred to as “∆NAGO1”. Interestingly, significant correlations between hypomethylation/activation of AGO1-V2 and hypermethylation/repression of AGO1 were observed upon examination of tumor cell lines and tissue datasets. Overall, our study reveals the existence of a process of interdependent epigenetic alterations in the AGO1 locus, which promotes swapping between two AGO1 protein-coding mRNA isoforms in tumors. Full article
(This article belongs to the Special Issue New Insights into Epigenetic Regulation in Cancer)
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Review

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17 pages, 1120 KiB  
Review
Oncogenic Roles of UHRF1 in Cancer
by Ahhyun Kim and Claudia A. Benavente
Epigenomes 2024, 8(3), 26; https://doi.org/10.3390/epigenomes8030026 - 1 Jul 2024
Viewed by 999
Abstract
Ubiquitin-like with PHD and RING finger domains 1 (UHRF1) is an essential protein involved in the maintenance of repressive epigenetic marks, ensuring epigenetic stability and fidelity. As an epigenetic regulator, UHRF1 comprises several functional domains (UBL, TTD, PHD, SRA, RING) that are collectively [...] Read more.
Ubiquitin-like with PHD and RING finger domains 1 (UHRF1) is an essential protein involved in the maintenance of repressive epigenetic marks, ensuring epigenetic stability and fidelity. As an epigenetic regulator, UHRF1 comprises several functional domains (UBL, TTD, PHD, SRA, RING) that are collectively responsible for processes like DNA methylation, histone modification, and DNA repair. UHRF1 is a downstream effector of the RB/E2F pathway, which is nearly universally deregulated in cancer. Under physiological conditions, UHRF1 protein levels are cell cycle-dependent and are post-translationally regulated by proteasomal degradation. Conversely, UHRF1 is overexpressed and serves as an oncogenic driver in multiple cancers. This review focuses on the functional domains of UHRF1, highlighting its key interacting proteins and oncogenic roles in solid tumors including retinoblastoma, osteosarcoma, lung cancer, and breast cancer. Additionally, current therapeutic strategies targeting UHRF1 domains or its interactors are explored, providing an insight on potential clinical applications. Full article
(This article belongs to the Special Issue New Insights into Epigenetic Regulation in Cancer)
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