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Molecular Research of DNA Methylation in Cancer Therapy
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Molecular Research of DNA Methylation in Cancer Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 2322

Special Issue Editor

Dr. Giovanni Cugliari

E-Mail Website
Guest Editor
Department of Medical Sciences, University of Turin, 10126 Turin, Italy
Interests: epigenetics; DNA methylation; cancer; statistical methods; artificial intelligence; machine learning; multi-omics analyses
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Crucial advances have recently been made in the understanding of molecular complex biology and the process of cancer development. Examples of these include the identification of new biomarkers and the deciphering of differences in DNA methylation, but these have not yet been established in clinical routine. Overall, there is no evidence of a real breakthrough in the treatment of several diseases. Further research and clinical trials are needed in order to evaluate outcomes and to identify new potential treatment candidates.

Given these improvements, novel risk assessment procedures and therapeutic strategies are being explored in order to (1) introduce the interaction between phenotypes and epigenetic-related variables to better characterize the cancer pathway, and (2) evaluate new causal approaches in order to investigate integromic strategies, including those employing more than one omics dataset simultaneously.

In this regard, many studies focused on the molecular aspects of cancer have been conducted worldwide, aiming to enhance our current understanding of tumor cell functioning, to describe the molecular mechanisms of therapeutic options, and to discover novel targets and drugs for cancer treatment.

This Special Issue aims to highlight recent advances in cancer research, with a particular emphasis on the molecular aspects of cancer. Thus, in order to provide a comprehensive overview of recent advances in cancer research, we invite researchers to submit original research papers and high-quality comprehensive reviews in the field of cancer research to this Special Issue. 

Dr. Giovanni Cugliari
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • DNA methylation
  • epigenetics
  • integromics
  • cancer
  • prognosis
  • treatment
  • early detection
  • gene therapy
  • machine learning
  • artificial intelligence
  • molecuplar pathway

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Published Papers (2 papers)

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Research

15 pages, 2054 KiB  
Article
Selective Estrogen Receptor Modulators’ (SERMs) Influence on TET3 Expression in Breast Cancer Cell Lines with Distinct Biological Subtypes
by Kinga Linowiecka, Justyna Szpotan, Marlena Godlewska, Damian Gaweł, Ewelina Zarakowska, Daniel Gackowski, Anna A. Brożyna and Marek Foksiński
Int. J. Mol. Sci. 2024, 25(16), 8561; https://doi.org/10.3390/ijms25168561 - 6 Aug 2024
Viewed by 829
Abstract
Tamoxifen, a selective estrogen receptor modulator (SERM), exhibits dual agonist or antagonist effects contingent upon its binding to either G-protein-coupled estrogen receptor (GPER) or estrogen nuclear receptor (ESR). Estrogen signaling plays a pivotal role in initiating epigenetic alterations and regulating estrogen-responsive genes in [...] Read more.
Tamoxifen, a selective estrogen receptor modulator (SERM), exhibits dual agonist or antagonist effects contingent upon its binding to either G-protein-coupled estrogen receptor (GPER) or estrogen nuclear receptor (ESR). Estrogen signaling plays a pivotal role in initiating epigenetic alterations and regulating estrogen-responsive genes in breast cancer. Employing three distinct breast cancer cell lines—MCF-7 (ESR+; GPER+), MDA-MB-231 (ESR−; GPER−), and SkBr3 (ESR−; GPER+)—this study subjected them to treatment with two tamoxifen derivatives: 4-hydroxytamoxifen (4-HT) and endoxifen (Endox). Through 2D high-performance liquid chromatography with tandem mass spectrometry detection (HPLC-MS/MS), varying levels of 5-methylcytosine (5-mC) were found, with MCF-7 displaying the highest levels. Furthermore, TET3 mRNA expression levels varied among the cell lines, with MCF-7 exhibiting the lowest expression. Notably, treatment with 4-HT induced significant changes in TET3 expression across all cell lines, with the most pronounced increase seen in MCF-7 and the least in MDA-MB-231. These findings underscore the influence of tamoxifen derivatives on DNA methylation patterns, particularly through modulating TET3 expression, which appears to be contingent on the presence of estrogen receptors. This study highlights the potential of targeting epigenetic modifications for personalized anti-cancer therapy, offering a novel avenue to improve treatment outcomes. Full article
(This article belongs to the Special Issue Molecular Research of DNA Methylation in Cancer Therapy)
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12 pages, 10878 KiB  
Article
Methylation-Based Characterization of a New IDH2 Mutation in Sinonasal Undifferentiated Carcinoma
by Simon Burgermeister, Simona Stoykova, Fanny S. Krebs, Vincent Zoete, Martial Mbefo, Kristof Egervari, Antoine Reinhard, Bettina Bisig and Ekkehard Hewer
Int. J. Mol. Sci. 2024, 25(12), 6518; https://doi.org/10.3390/ijms25126518 - 13 Jun 2024
Viewed by 1082
Abstract
Mutations affecting codon 172 of the isocitrate dehydrogenase 2 (IDH2) gene define a subgroup of sinonasal undifferentiated carcinomas (SNUCs) with a relatively favorable prognosis and a globally hypermethylated phenotype. They are also recurrent (along with IDH1 mutations) in gliomas, acute myeloid [...] Read more.
Mutations affecting codon 172 of the isocitrate dehydrogenase 2 (IDH2) gene define a subgroup of sinonasal undifferentiated carcinomas (SNUCs) with a relatively favorable prognosis and a globally hypermethylated phenotype. They are also recurrent (along with IDH1 mutations) in gliomas, acute myeloid leukemia, and intrahepatic cholangiocarcinoma. Commonly reported mutations, all associated with aberrant IDH2 enzymatic activity, include R172K, R172S, R172T, R172G, and R172M. We present a case of SNUC with a never-before-described IDH2 mutation, R172A. Our report compares the methylation pattern of our sample to other cases from the Gene Expression Omnibus database. Hierarchical clustering suggests a strong association between our sample and other IDH-mutant SNUCs and a clear distinction between sinonasal normal tissues and tumors. Principal component analysis (PCA), using 100 principal components explaining 94.5% of the variance, showed the position of our sample to be within 1.02 standard deviation of the other IDH-mutant SNUCs. A molecular modeling analysis of the IDH2 R172A versus other R172 variants provides a structural explanation to how they affect the protein active site. Our findings thus suggest that the R172A mutation in IDH2 confers a gain of function similar to other R172 mutations in IDH2, resulting in a similar hypermethylated profile. Full article
(This article belongs to the Special Issue Molecular Research of DNA Methylation in Cancer Therapy)
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