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Epigenetic Modifications and Carcinogenesis
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Epigenetic Modifications and Carcinogenesis

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 (30 April 2021) | Viewed by 7061

Special Issue Editor

Dr. Ashakumary Lakshmikuttyamma

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, Jefferson College of Pharmacy, Thomas Jefferson University, Philadelphia, PA 19107, USA
Interests: breast cancer; tumor suppressor genes; epigenetics; natural products
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The association between epigenetic changes and carcinogenesis has been well established. DNA methylation and histone modifications are common epigenetic alterations associated with cancer development and metastasis. Various tumor suppressor genes and oncogenes are regulated by epigenetic alterations. Different epigenetic modifiers are currently used as anti-cancer drugs, and a large number of drugs under this category are currently involved in clinical trials for various cancers. Recently, microRNAs and noncoding RNAs attained significant importance in carcinogenesis. Various miRNAs and noncoding RNAs are detected as biomarkers for the progression of different cancers, which can be considered as potential therapeutic targets. Different anti-sense nucleotides targeting microRNAs and noncoding RNAs are in clinical trials to treat cancer.

Either evidence-based original research, or a review of the scientific literature of any topic related to epigenetics and cancer, are welcome for this Special Issue.

Dr. Ashakumary Lakshmikuttyamma
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

  • Epigenetics
  • Tumor suppressor genes
  • DNA methylation
  • Histone modification
  • DNA methyltransferase
  • Histone deacetylase
  • Histone acyltransferase
  • MicroRNA
  • Noncoding RNA
  • Carcinogenesis

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Published Papers (2 papers)

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21 pages, 2754 KiB  
Article
Epigenetic DNA Methylation of EBI3 Modulates Human Interleukin-35 Formation via NFkB Signaling: A Promising Therapeutic Option in Ulcerative Colitis
by Alexandra Wetzel, Bettina Scholtka, Fabian Schumacher, Harshadrai Rawel, Birte Geisendörfer and Burkhard Kleuser
Int. J. Mol. Sci. 2021, 22(10), 5329; https://doi.org/10.3390/ijms22105329 - 19 May 2021
Cited by 11 | Viewed by 3225
Abstract
Ulcerative colitis (UC), a severe chronic disease with unclear etiology that is associated with increased risk for colorectal cancer, is accompanied by dysregulation of cytokines. Epstein–Barr virus-induced gene 3 (EBI3) encodes a subunit in the unique heterodimeric IL-12 cytokine family of [...] Read more.
Ulcerative colitis (UC), a severe chronic disease with unclear etiology that is associated with increased risk for colorectal cancer, is accompanied by dysregulation of cytokines. Epstein–Barr virus-induced gene 3 (EBI3) encodes a subunit in the unique heterodimeric IL-12 cytokine family of either pro- or anti-inflammatory function. After having recently demonstrated that upregulation of EBI3 by histone acetylation alleviates disease symptoms in a dextran sulfate sodium (DSS)-treated mouse model of chronic colitis, we now aimed to examine a possible further epigenetic regulation of EBI3 by DNA methylation under inflammatory conditions. Treatment with the DNA methyltransferase inhibitor (DNMTi) decitabine (DAC) and TNFα led to synergistic upregulation of EBI3 in human colon epithelial cells (HCEC). Use of different signaling pathway inhibitors indicated NFκB signaling was necessary and proportional to the synergistic EBI3 induction. MALDI-TOF/MS and HPLC-ESI-MS/MS analysis of DAC/TNFα-treated HCEC identified IL-12p35 as the most probable binding partner to form a functional protein. EBI3/IL-12p35 heterodimers (IL-35) induce their own gene upregulation, something that was indeed observed in HCEC cultured with media from previously DAC/TNFα-treated HCEC. These results suggest that under inflammatory and demethylating conditions the upregulation of EBI3 results in the formation of anti-inflammatory IL-35, which might be considered as a therapeutic target in colitis. Full article
(This article belongs to the Special Issue Epigenetic Modifications and Carcinogenesis)
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16 pages, 2272 KiB  
Article
Global Analyses of Expressed Piwi-Interacting RNAs in Gastric Cancer
by Tatiana Vinasco-Sandoval, Fabiano Cordeiro Moreira, Amanda F. Vidal, Pablo Pinto, André M. Ribeiro-dos-Santos, Rebecca L. S. Cruz, Gleyce Fonseca Cabral, Ana K. M. Anaissi, Katia de Paiva Lopes, Arthur Ribeiro-dos-Santos, Samia Demachki, Paulo Pimentel de Assumpção, Ândrea Ribeiro-dos-Santos and Sidney Santos
Int. J. Mol. Sci. 2020, 21(20), 7656; https://doi.org/10.3390/ijms21207656 - 16 Oct 2020
Cited by 11 | Viewed by 3336
Abstract
Gastric cancer (GC) represents a notable amount of morbidity and mortality worldwide. Understanding the molecular basis of CG will offer insight into its pathogenesis in an attempt to identify new molecular biomarkers to early diagnose this disease. Therefore, studies involving small non-coding RNAs [...] Read more.
Gastric cancer (GC) represents a notable amount of morbidity and mortality worldwide. Understanding the molecular basis of CG will offer insight into its pathogenesis in an attempt to identify new molecular biomarkers to early diagnose this disease. Therefore, studies involving small non-coding RNAs have been widely explored. Among these, PIWI-interacting RNAs (piRNAs) are an emergent class that can play important roles in carcinogenesis. In this study, small-RNA sequencing was used to identify the global piRNAs expression profile (piRNome) of gastric cancer patients. We found 698 piRNAs in gastric tissues, 14 of which were differentially expressed (DE) between gastric cancer (GC), adjacent to gastric cancer (ADJ), and non-cancer tissues (NC). Moreover, three of these DE piRNAs (piR-48966*, piR-49145, piR-31335*) were differently expressed in both GC and ADJ samples in comparison to NC samples, indicating that the tumor-adjacent tissue was molecularly altered and should not be considered as a normal control. These three piRNAs are potential risk biomarkers for GC, especially piR-48966* and piR-31335*. Furthermore, an in-silico search for mRNAs targeted by the differentially expressed piRNAs revealed that these piRNAs may regulate genes that participate in cancer-related pathways, suggesting that these small non-coding RNAs may be directly and indirectly involved in gastric carcinogenesis. Full article
(This article belongs to the Special Issue Epigenetic Modifications and Carcinogenesis)
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