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Cancers
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Advances in Cancer Epigenetics
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Advances in Cancer Epigenetics

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 14839

Special Issue Editors

Prof. Dr. Noël J. Raynal

E-Mail Website
Guest Editor
Département de Pharmacologie et de Physiologie, Université de Montréal and Sainte-Justine University Hospital Research Center, Montréal, QC, Canada
Interests: cancer epigenetics; chromatin; DNA methylation; epigenetic drugs; in vitro models; drug screening
Prof. Dr. Serge McGraw

E-Mail Website
Guest Editor
1. Department of Biochemistry and Molecular Medicine, Université de Montréal, Montreal, QC, Canada
2. Centre de recherche du CHU Sainte-Justine, Montreal, QC, Canada
3. Department of Obstetrics and Gynecology, Université de Montréal, Montreal, QC, Canada
Interests: epigenetics; DNA methylation; bioinformatics

Special Issue Information

Dear Colleagues, 

The alteration of the epigenome profiles is a hallmark of virtually all cancers. New advances in cancer epigenetics highlight the complexity and intricacy of various epigenetic modifications from early steps of neoplasia, cancer stem cell maintenance, and metastasis. The importance of metabolism alterations and toxicant exposure play a clear role in carcinogenesis and response to therapy. The understating of the coordination between active and repressive epigenetic marks has increased considerably in recent years and leads to tailored epigenetic therapeutics, which represent the future of precision medicine.

Prof. Dr. Noël J. Raynal
Prof. Dr. Serge McGraw
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 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. Cancers 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 2900 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
  • histone modification
  • DNA methylation
  • epigenetic therapy of cancer
  • cancer metabolism and epigenetics

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Published Papers (5 papers)

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Research

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26 pages, 7163 KiB  
Article
Notch, SUMOylation, and ESR-Mediated Signalling Are the Main Molecular Pathways Showing Significantly Different Epimutation Scores between Expressing or Not Oestrogen Receptor Breast Cancer in Three Public EWAS Datasets
by Luigi Corsaro, Davide Gentilini, Luciano Calzari and Vincenzo Sandro Gambino
Cancers 2023, 15(16), 4109; https://doi.org/10.3390/cancers15164109 - 15 Aug 2023
Cited by 1 | Viewed by 1585 | Correction
Abstract
Oestrogen receptor expression in breast cancer (BC) cells is a marker of high cellular differentiation and allows the identification of two BC groups (ER-positive and ER-negative) that, although not completely homogeneous, differ in biological characteristics, clinical behaviour, and therapeutic options. The study, based [...] Read more.
Oestrogen receptor expression in breast cancer (BC) cells is a marker of high cellular differentiation and allows the identification of two BC groups (ER-positive and ER-negative) that, although not completely homogeneous, differ in biological characteristics, clinical behaviour, and therapeutic options. The study, based on three publicly available EWAS (Epigenetic Wide Association Study) datasets, focuses on the comparison between these two groups of breast cancer using an epimutation score. The score is calculated not only based on the presence of the epimutation, but also on the deviation amplitude of the methylation outlier value. For each dataset, we performed a functional analysis based first on the functional gene region of each annotated gene (we aggregated the data per gene region TSS1500, TSS200, first-exon, and body-gene identified by the information from the Illumina Data Sheet), and then, we performed a pathway enrichment analysis through the REACTOME database based on the genes with the highest epimutation score. Thus, we blended our results and found common pathways for all three datasets. We found that a higher and significant epimutation score due to hypermethylation in ER-positive BC is present in the promoter region of the genes belonging to the SUMOylation pathway, the Notch pathway, the IFN-γ signalling pathway, and the deubiquitination protease pathway, while a higher and significant level of epimutation due to hypomethylation in ER-positive BC is present in the promoter region of the genes belonging to the ESR-mediated pathway. The presence of this state of promoter hypomethylation in the ESR-mediated signalling genes is consistent and coherent with an active signalling pathway mediated by oestrogen function in the group of ER-positive BC. The SUMOylation and Notch pathways are associated with BC pathogenesis and have been found to play distinct roles in the two BC subgroups. We speculated that the altered methylation profile may play a role in regulating signalling pathways with specific functions in the two subgroups of ER BC. Full article
(This article belongs to the Special Issue Advances in Cancer Epigenetics)
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23 pages, 5614 KiB  
Article
Resistance of Leukemia Cells to 5-Azacytidine: Different Responses to the Same Induction Protocol
by Kristína Šimoničová, Lubos Janotka, Helena Kavcova, Zdena Sulova, Lucia Messingerova and Albert Breier
Cancers 2023, 15(11), 3063; https://doi.org/10.3390/cancers15113063 - 5 Jun 2023
Cited by 2 | Viewed by 2384
Abstract
Three AML cell variants (M/A, M/A* from MOLM-13 and S/A from SKM-1) were established for resistance by the same protocol using 5-azacytidine (AZA) as a selection agent. These AZA-resistant variants differ in their responses to other cytosine nucleoside analogs, including 5-aza-2′-deoxycytidine (DAC), as [...] Read more.
Three AML cell variants (M/A, M/A* from MOLM-13 and S/A from SKM-1) were established for resistance by the same protocol using 5-azacytidine (AZA) as a selection agent. These AZA-resistant variants differ in their responses to other cytosine nucleoside analogs, including 5-aza-2′-deoxycytidine (DAC), as well as in some molecular features. Differences in global DNA methylation, protein levels of DNA methyltransferases, and phosphorylation of histone H2AX were observed in response to AZA and DAC treatment in these cell variants. This could be due to changes in the expression of uridine-cytidine kinases 1 and 2 (UCK1 and UCK2) demonstrated in our cell variants. In the M/A variant that retained sensitivity to DAC, we detected a homozygous point mutation in UCK2 resulting in an amino acid substitution (L220R) that is likely responsible for AZA resistance. Cells administered AZA treatment can switch to de novo synthesis of pyrimidine nucleotides, which could be blocked by inhibition of dihydroorotate dehydrogenase by teriflunomide (TFN). This is shown by the synergistic effect of AZA and TFN in those variants that were cross-resistant to DAC and did not have a mutation in UCK2. Full article
(This article belongs to the Special Issue Advances in Cancer Epigenetics)
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22 pages, 3382 KiB  
Article
Selective CDK9 Inhibition by Natural Compound Toyocamycin in Cancer Cells
by Somnath Pandey, Rahinatou Djibo, Anaïs Darracq, Gennaro Calendo, Hanghang Zhang, Ryan A. Henry, Andrew J. Andrews, Stephen B. Baylin, Jozef Madzo, Rafael Najmanovich, Jean-Pierre J. Issa and Noël J.-M. Raynal
Cancers 2022, 14(14), 3340; https://doi.org/10.3390/cancers14143340 - 8 Jul 2022
Cited by 11 | Viewed by 3798
Abstract
Aberrant transcription in cancer cells involves the silencing of tumor suppressor genes (TSGs) and activation of oncogenes. Transcriptomic changes are associated with epigenomic alterations such as DNA-hypermethylation, histone deacetylation, and chromatin condensation in promoter regions of silenced TSGs. To discover novel drugs that [...] Read more.
Aberrant transcription in cancer cells involves the silencing of tumor suppressor genes (TSGs) and activation of oncogenes. Transcriptomic changes are associated with epigenomic alterations such as DNA-hypermethylation, histone deacetylation, and chromatin condensation in promoter regions of silenced TSGs. To discover novel drugs that trigger TSG reactivation in cancer cells, we used a GFP-reporter system whose expression is silenced by promoter DNA hypermethylation and histone deacetylation. After screening a natural product drug library, we identified that toyocamycin, an adenosine-analog, induces potent GFP reactivation and loss of clonogenicity in human colon cancer cells. Connectivity-mapping analysis revealed that toyocamycin produces a pharmacological signature mimicking cyclin-dependent kinase (CDK) inhibitors. RNA-sequencing revealed that the toyocamycin transcriptomic signature resembles that of a specific CDK9 inhibitor (HH1). Specific inhibition of RNA Pol II phosphorylation level and kinase assays confirmed that toyocamycin specifically inhibits CDK9 (IC50 = 79 nM) with a greater efficacy than other CDKs (IC50 values between 0.67 and 15 µM). Molecular docking showed that toyocamycin efficiently binds the CDK9 catalytic site in a conformation that differs from other CDKs, explained by the binding contribution of specific amino acids within the catalytic pocket and protein backbone. Altogether, we demonstrated that toyocamycin exhibits specific CDK9 inhibition in cancer cells, highlighting its potential for cancer chemotherapy. Full article
(This article belongs to the Special Issue Advances in Cancer Epigenetics)
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Review

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27 pages, 3532 KiB  
Review
Prospective Epigenetic Actions of Organo-Sulfur Compounds against Cancer: Perspectives and Molecular Mechanisms
by Shoaib Shoaib, Mohammad Azam Ansari, Mohammed Ghazwani, Umme Hani, Yahya F. Jamous, Zahraa Alali, Shadma Wahab, Wasim Ahmad, Sydney A. Weir, Mohammad N. Alomary, Nabiha Yusuf and Najmul Islam
Cancers 2023, 15(3), 697; https://doi.org/10.3390/cancers15030697 - 23 Jan 2023
Cited by 11 | Viewed by 3550
Abstract
Major epigenetic alterations, such as chromatin modifications, DNA methylation, and miRNA regulation, have gained greater attention and play significant roles in oncogenesis, representing a new paradigm in our understanding of cancer susceptibility. These epigenetic changes, particularly aberrant promoter hypermethylation, abnormal histone acetylation, and [...] Read more.
Major epigenetic alterations, such as chromatin modifications, DNA methylation, and miRNA regulation, have gained greater attention and play significant roles in oncogenesis, representing a new paradigm in our understanding of cancer susceptibility. These epigenetic changes, particularly aberrant promoter hypermethylation, abnormal histone acetylation, and miRNA dysregulation, represent a set of epigenetic patterns that contribute to inappropriate gene silencing at every stage of cancer progression. Notably, the cancer epigenome possesses various HDACs and DNMTs, which participate in the histone modifications and DNA methylation. As a result, there is an unmet need for developing the epigenetic inhibitors against HDACs and DNMTs for cancer therapy. To date, several epigenetically active synthetic inhibitors of DNA methyltransferases and histone deacetylases have been developed. However, a growing body of research reports that most of these synthetic inhibitors have significant side effects and a narrow window of specificity for cancer cells. Targeting tumor epigenetics with phytocompounds that have the capacity to modulate abnormal DNA methylation, histone acetylation, and miRNAs expression is one of the evolving strategies for cancer prevention. Encouragingly, there are many bioactive phytochemicals, including organo-sulfur compounds that have been shown to alter the expression of key tumor suppressor genes, oncogenes, and oncogenic miRNAs through modulation of DNA methylation and histones in cancer. In addition to vitamins and microelements, dietary phytochemicals such as sulforaphane, PEITC, BITC, DADS, and allicin are among a growing list of naturally occurring anticancer agents that have been studied as an alternative strategy for cancer treatment and prevention. Moreover, these bioactive organo-sulfur compounds, either alone or in combination with other standard cancer drugs or phytochemicals, showed promising results against many cancers. Here, we particularly summarize and focus on the impact of specific organo-sulfur compounds on DNA methylation and histone modifications through targeting the expression of different DNMTs and HDACs that are of particular interest in cancer therapy and prevention. Full article
(This article belongs to the Special Issue Advances in Cancer Epigenetics)
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24 pages, 1843 KiB  
Review
Long Non-Coding RNAs as Epigenetic Regulators of Immune Checkpoints in Cancer Immunity
by Wiam Saadi, Ahlam Fatmi, Federico V. Pallardó, José Luis García-Giménez and Salvador Mena-Molla
Cancers 2023, 15(1), 184; https://doi.org/10.3390/cancers15010184 - 28 Dec 2022
Cited by 6 | Viewed by 2367
Abstract
In recent years, cancer treatment has undergone significant changes, predominantly in the shift towards immunotherapeutic strategies using immune checkpoint inhibitors. Despite the clinical efficacy of many of these inhibitors, the overall response rate remains modest, and immunotherapies for many cancers have proved ineffective, [...] Read more.
In recent years, cancer treatment has undergone significant changes, predominantly in the shift towards immunotherapeutic strategies using immune checkpoint inhibitors. Despite the clinical efficacy of many of these inhibitors, the overall response rate remains modest, and immunotherapies for many cancers have proved ineffective, highlighting the importance of knowing the tumor microenvironment and heterogeneity of each malignancy in patients. Long non-coding RNAs (lncRNAs) have attracted increasing attention for their ability to control various biological processes by targeting different molecular pathways. Some lncRNAs have a regulatory role in immune checkpoints, suggesting they might be utilized as a target for immune checkpoint treatment. The focus of this review is to describe relevant lncRNAs and their targets and functions to understand key regulatory mechanisms that may contribute in regulating immune checkpoints. We also provide the state of the art on super-enhancers lncRNAs (selncRNAs) and circular RNAs (circRNAs), which have recently been reported as modulators of immune checkpoint molecules within the framework of human cancer. Other feasible mechanisms of interaction between lncRNAs and immune checkpoints are also reported, along with the use of miRNAs and circRNAs, in generating new tumor immune microenvironments, which can further help avoid tumor evasion. Full article
(This article belongs to the Special Issue Advances in Cancer Epigenetics)
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