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Biomedicines
Special Issues
Epigenetics in Cancer and the Therapeutic Potential of Epi-Drugs
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Epigenetics in Cancer and the Therapeutic Potential of Epi-Drugs

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 4506

Special Issue Editors

Dr. Sonia Emanuele

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Guest Editor
Department of Biomedicine, Neurosciences and Advanced Diagnostics (BIND), Biochemistry Building, University of Palermo, 90127 Palermo, Italy
Interests: apoptosis; cancer; autophagy; epigenetics; HDAC inhibitors; cell stress
Special Issues, Collections and Topics in MDPI journals
Dr. Antonietta Notaro

E-Mail Website
Guest Editor
Department of Biological, Chemical and Pharmaceutical Sciences and Technologies (STEBICEF), University of Palermo, 90127 Palermo, Italy
Interests: cancer; cell death mechanisms; nutraceuticals; oxidative stress; neurochemistry
Dr. Adriana Celesia

E-Mail Website
Guest Editor
1. Department of Neurosciences, Biomedicine and Movement Sciences, Biological Chemistry Section, University of Verona, 37134 Verona, Italy
2. Department of Biomedicine, Neurosciences and Advanced Diagnostics (BIND), Biochemistry Building, University of Palermo, 90127 Palermo, Italy
Interests: cancer; epigenetics; cell death; biochemistry; molecular biology

Special Issue Information

Dear Colleagues,

The study of epigenetics has profoundly modified the perception of how behaviors and the environment influence cell fate and overall human health. Epigenetics refers to a wide set of transcriptional regulation mechanisms that do not depend on gene sequence. These mechanisms include chromatin modifications, such as DNA methylation and covalent histone modifications, variations in nucleosome positioning along DNA, and long noncoding RNAs (LncRNAs) regulation. Recent progress in epigenetics has indicated that cancer cells display genetic mutations and epigenetic abnormalities, accounting for tumor development and progression. It is widely recognized that changes in the epigenetic landscape can be considered a hallmark of cancer. Therefore, the modulation of epigenetic modifications represents a strategy to selectively target tumor cells. It is not by chance that epigenetic compounds, such as histone deacetylase (HDAC) inhibitors or DNA demethylating agents, have been developed and used as antitumor drugs either in vitro or in vivo; some of these compounds have already entered clinical trials and showed a certain efficacy. Moreover, lncRNAs are key regulators of the epigenetic status of the human genome and profoundly influence tumor transformation and development. The aim of this Special Issue is to focus on the molecular mechanisms of epigenetic regulation in cancer and to describe possible therapeutic approaches based on using epigenetic compounds or modulation of lncRNAs. In addition, this Special Issue aims to provide the molecular characterization of the action mechanisms induced by epigenetic compounds, including HDAC inhibitors, demethylating agents, or other drugs modulating the histone code, influencing LncRNAs expression or acting on nucleosome positioning.

Prof. Dr. Sonia Emanuele
Dr. Antonietta Notaro
Dr. Adriana Celesia
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. Biomedicines 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

  • epigenetics
  • cancer
  • HDAC inhibitors
  • DNMT inhibitors
  • nucleosomes
  • histone code
  • apoptosis

Published Papers (2 papers)

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Research

12 pages, 978 KiB  
Article
Epigenetic Suppression of the IL-7 Pathway in Progressive Glioblastoma
by Marton Tompa, Zoltan Kraboth, Bence Galik, Bela Kajtar, Attila Gyenesei and Bernadette Kalman
Biomedicines 2022, 10(9), 2174; https://doi.org/10.3390/biomedicines10092174 - 02 Sep 2022
Cited by 2 | Viewed by 2013
Abstract
Background: Immune evasion in glioblastoma (GBM) shields cancer cells from cytotoxic immune response. Methods: We investigated CpG methylation in promoters, genes, and pathways in 22 pairs of formalin-fixed paraffin-embedded sequential (FFPE) GBM using restricted resolution bisulfite sequencing (RRBS) and bioinformatic analyses. Results: Gene [...] Read more.
Background: Immune evasion in glioblastoma (GBM) shields cancer cells from cytotoxic immune response. Methods: We investigated CpG methylation in promoters, genes, and pathways in 22 pairs of formalin-fixed paraffin-embedded sequential (FFPE) GBM using restricted resolution bisulfite sequencing (RRBS) and bioinformatic analyses. Results: Gene ontology revealed hypermethylation in elements of the innate and adaptive immune system when recurrent GBM samples (GBMrec) were compared to control (CG) and primary GBM samples (GBMprim). Higher methylation levels of the IL-7 signaling pathway and response to IL-7 were found in GBMrec suggesting a progressive blockade of the IL-7 driven T cell response in sequential GBM. Analyses of the Cancer Genome Atlas array-based data confirmed hypermethylation of the IL-7 pathway in recurrent compared with primary GBM. We also quantified DNA CpG methylation in promoter and gene regions of the IL-7 ligand and IL-7 α-receptor subunit in individual samples of a large RRBS-based sequential cohort of GBM in a Viennese database and found significantly higher methylation levels in the IL-7 receptor α-subunit in GBMrec compared with GBMprim. Conclusions: This study revealed the progressive suppression of the IL-7 receptor-mediated pathway as a means of immune evasion by GBM and thereby highlighted it as a new treatment target. Full article
(This article belongs to the Special Issue Epigenetics in Cancer and the Therapeutic Potential of Epi-Drugs)
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17 pages, 3284 KiB  
Article
The Histone Deacetylase Inhibitor ITF2357 (Givinostat) Targets Oncogenic BRAF in Melanoma Cells and Promotes a Switch from Pro-Survival Autophagy to Apoptosis
by Adriana Celesia, Antonietta Notaro, Marzia Franzò, Marianna Lauricella, Antonella D’Anneo, Daniela Carlisi, Michela Giuliano and Sonia Emanuele
Biomedicines 2022, 10(8), 1994; https://doi.org/10.3390/biomedicines10081994 - 17 Aug 2022
Cited by 3 | Viewed by 1451
Abstract
Histone deacetylase inhibitors (HDACI) are epigenetic compounds that have been widely considered very promising antitumor agents. Here, we focus on the effects of the pan-HDAC inhibitor ITF2357 (Givinostat) in comparison with SAHA (Vorinostat) in melanoma cells bearing BRAF V600E oncogenic mutation. Our results [...] Read more.
Histone deacetylase inhibitors (HDACI) are epigenetic compounds that have been widely considered very promising antitumor agents. Here, we focus on the effects of the pan-HDAC inhibitor ITF2357 (Givinostat) in comparison with SAHA (Vorinostat) in melanoma cells bearing BRAF V600E oncogenic mutation. Our results indicate both ITF2357 and SAHA dose-dependently reduce the viability of BRAF-mutated SK-MEL-28 and A375 melanoma cells. The comparison of IC50 values revealed that ITF2357 was much more effective than SAHA. Interestingly, both inhibitors markedly decreased oncogenic BRAF protein expression levels, ITF2357 being the most effective compound. Moreover, the BRAF decrease induced by ITF2357 was accompanied by a decrease in the level of phospho-ERK1/2. The inhibitor of upstream MEK activity, U0126, reduced ERK1/2 phosphorylation and dramatically potentiated the antitumor effect of ITF2357, exacerbating the reduction in the BRAF level. ITF2357 stimulated an early pro-survival autophagic response, which was followed by apoptosis, as indicated by apoptotic markers evaluation and the protective effects exerted by the pan-caspase inhibitor z-VADfmk. Overall, our data indicate for the first time that ITF2357 targets oncogenic BRAF in melanoma cells and induces a switch from autophagy to classic apoptosis, thus representing a possible candidate in melanoma targeted therapy. Full article
(This article belongs to the Special Issue Epigenetics in Cancer and the Therapeutic Potential of Epi-Drugs)
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