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Cells
Special Issues
Navigating Through the Epigenetic Pathways of Cancer
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Navigating Through the Epigenetic Pathways of Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Nuclei: Function, Transport and Receptors".

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 16819

Special Issue Editor

Dr. Maria Hatziapostolou

E-Mail Website
Guest Editor
Department of Biosciences, The John van Geest Cancer Research Centre, Nottingham Trent University, Nottingham NG11 8NS, UK
Interests: de-regulated non-coding RNAs in gastrointestinal cancers; DNA methylation in pancreatic cancer; targeting long non-coding RNAs for cancer treatment; mechanisms of chemoresistance in hepatocellular carcinoma; cancer progression and metastasis; tumour-stroma interactions; systems biology; high-throughput approaches.
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The term epigenetics defines heritable phenotypic changes that are not encoded in the sequence of the genome. Epigenetic alterations control gene expression at the transcriptional and/or post-transcriptional level. There are three main epigenetic mechanisms: DNA methylation, histone modifications, and non-coding RNAs. It is now established that epigenetic changes work in concert with genetics for the initiation, growth, and aggressiveness of many cancer types.

The reversible nature of epigenetic modifications revolutionized cancer therapeutics and reinforced the design and development of epigenetic-altering drugs. Furthermore, non-coding RNAs (microRNAs and long non-coding RNAs) have emerged as novel attractive therapeutic targets due to their ability to control gene expression, affect a plethora of cellular properties, and interact with other parts of the epigenetic machinery. Importantly, recent data indicate that DNA methylation patterns and non-coding RNA profiles could serve as biomarkers for disease diagnosis, prognosis and response to a treatment.

The purpose of this Special Issue is to focus on cutting-edge research, across a wide range of topics, relevant to cancer epigenetics. We invite authors to submit original, meta-analyses, and review articles on basic research, translational, and cancer diagnosis or treatment.

Dr. Maria Hatziapostolou
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • DNA methylation
  • Histone modifications
  • Non-coding RNAs (miRNAs, lncRNAs)
  • Epigenetic mechanisms
  • Biomarkers
  • Cancer treatment
  • Inflammation

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Published Papers (3 papers)

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23 pages, 6676 KiB  
Article
Adjuvant Epigenetic Therapy of Decitabine and Suberoylanilide Hydroxamic Acid Exerts Anti-Neoplastic Effects in Acute Myeloid Leukemia Cells
by Sonia Abou Najem, Ghada Khawaja, Mohammad Hassan Hodroj, Patil Babikian and Sandra Rizk
Cells 2019, 8(12), 1480; https://doi.org/10.3390/cells8121480 - 21 Nov 2019
Cited by 11 | Viewed by 4525
Abstract
Atypical epigenetic processes including histone acetylation and DNA methylation have been identified as a fundamental theme in hematologic malignancies. Such mechanisms modify gene expression and prompt, in part at least, the initiation and progression of several malignancies including acute myeloid leukemia. In the [...] Read more.
Atypical epigenetic processes including histone acetylation and DNA methylation have been identified as a fundamental theme in hematologic malignancies. Such mechanisms modify gene expression and prompt, in part at least, the initiation and progression of several malignancies including acute myeloid leukemia. In the current study we determined the effects of treating KG-1 and U937 acute myeloid leukemia (AML) cells, in vitro, with the HDAC inhibitor, suberoylanilide hydroxamic acid (SAHA), or with a DNMT inhibitor, decitabine (DAC), or their combination, on cell proliferation, cell cycle progression, apoptosis, and expression of apoptosis-related proteins. Each of SAHA and DAC attenuated cell proliferation and induced cell cycle arrest and apoptotic cell death of KG-1 and U937 cell lines. Besides, their sequential combination improved the obtained anti-neoplastic effect: significant augmentation of growth inhibition and apoptosis induction as compared to cells treated with either drug alone. This effect was featured by the upregulated expression of Bax, cytochrome c1, p21, and cleaved caspases 8, 9, and 3, signifying the activation of both the intrinsic and extrinsic pathways of apoptosis. The sequential combination of SAHA and DAC causes a profound antitumorigenic effect in AML cell lines by inducing the expression of tumor suppressor genes. Full article
(This article belongs to the Special Issue Navigating Through the Epigenetic Pathways of Cancer)
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Review

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37 pages, 958 KiB  
Review
Novel Epigenetic Biomarkers in Pregnancy-Related Disorders and Cancers
by Valentina Karin-Kujundzic, Ida Marija Sola, Nina Predavec, Anamarija Potkonjak, Ema Somen, Pavao Mioc, Alan Serman, Semir Vranic and Ljiljana Serman
Cells 2019, 8(11), 1459; https://doi.org/10.3390/cells8111459 - 18 Nov 2019
Cited by 13 | Viewed by 5768
Abstract
As the majority of cancers and gestational diseases are prognostically stage- and grade-dependent, the ultimate goal of ongoing studies in precision medicine is to provide early and timely diagnosis of such disorders. These studies have enabled the development of various new diagnostic biomarkers, [...] Read more.
As the majority of cancers and gestational diseases are prognostically stage- and grade-dependent, the ultimate goal of ongoing studies in precision medicine is to provide early and timely diagnosis of such disorders. These studies have enabled the development of various new diagnostic biomarkers, such as free circulating nucleic acids, and detection of their epigenetic changes. Recently, extracellular vesicles including exosomes, microvesicles, oncosomes, and apoptotic bodies have been recognized as powerful diagnostic tools. Extracellular vesicles carry specific proteins, lipids, DNAs, mRNAs, and miRNAs of the cells that produced them, thus reflecting the function of these cells. It is believed that exosomes, in particular, may be the optimal biomarkers of pathological pregnancies and cancers, especially those that are frequently diagnosed at an advanced stage, such as ovarian cancer. In the present review, we survey and critically appraise novel epigenetic biomarkers related to free circulating nucleic acids and extracellular vesicles, focusing especially on their status in trophoblasts (pregnancy) and neoplastic cells (cancers). Full article
(This article belongs to the Special Issue Navigating Through the Epigenetic Pathways of Cancer)
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30 pages, 2319 KiB  
Review
Epigenetic Regulation of Inflammatory Cytokine-Induced Epithelial-To-Mesenchymal Cell Transition and Cancer Stem Cell Generation
by Georgios S. Markopoulos, Eugenia Roupakia, Kenneth B. Marcu and Evangelos Kolettas
Cells 2019, 8(10), 1143; https://doi.org/10.3390/cells8101143 - 25 Sep 2019
Cited by 64 | Viewed by 6005
Abstract
The neoplastic transformation of normal to metastatic cancer cells is a complex multistep process involving the progressive accumulation of interacting genetic and epigenetic changes that alter gene function and affect cell physiology and homeostasis. Epigenetic changes including DNA methylation, histone modifications and changes [...] Read more.
The neoplastic transformation of normal to metastatic cancer cells is a complex multistep process involving the progressive accumulation of interacting genetic and epigenetic changes that alter gene function and affect cell physiology and homeostasis. Epigenetic changes including DNA methylation, histone modifications and changes in noncoding RNA expression, and deregulation of epigenetic processes can alter gene expression during the multistep process of carcinogenesis. Cancer progression and metastasis through an ‘invasion–metastasis cascade’ involving an epithelial-to-mesenchymal cell transition (EMT), the generation of cancer stem cells (CSCs), invasion of adjacent tissues, and dissemination are fueled by inflammation, which is considered a hallmark of cancer. Chronic inflammation is generated by inflammatory cytokines secreted by the tumor and the tumor-associated cells within the tumor microenvironment. Inflammatory cytokine signaling initiates signaling pathways leading to the activation of master transcription factors (TFs) such as Smads, STAT3, and NF-κB. Moreover, the same inflammatory responses also activate EMT-inducing TF (EMT-TF) families such as Snail, Twist, and Zeb, and epigenetic regulators including DNA and histone modifying enzymes and micoRNAs, through complex interconnected positive and negative feedback loops to regulate EMT and CSC generation. Here, we review the molecular regulatory feedback loops and networks involved in inflammatory cytokine-induced EMT and CSC generation. Full article
(This article belongs to the Special Issue Navigating Through the Epigenetic Pathways of Cancer)
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