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Cells
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Cancer Epigenetics: From Mechanism to Therapy
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Cancer Epigenetics: From Mechanism to Therapy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Proliferation and Division".

Deadline for manuscript submissions: closed (15 June 2022) | Viewed by 4856

Special Issue Editor

Prof. Dr. Pierre-Olivier Angrand

E-Mail Website1 Website2
Guest Editor
Université de Lille, CNRS, INSERM, CHU Lille, Centre Oscar Lambret, UMR 9020–UMR 1277–Canther–Cancer Heterogeneity, Plasticity and Resistance to Therapies, F-59000 Lille, France
Interests: epigenetics; zebrafish model; cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Although the genomic sequence of an organism encodes the primary information, additional information is added by epigenetic regulation. Epigenetic modulators include methylation of DNA, post-translational modifications of histones, incorporation of histone variants, non-coding RNAs, and the chromatin structure itself. Growing evidence has implicated the involvement of epigenetic alterations in cancer. Hence, epigenetic factors could serve as biomarkers for oncological diagnosis, prognosis, and as targets for cancer therapy.

The goal of this Special Issue on “Cancer Epigenetics” is to present the current knowledge on the involvement of epigenetic alterations in cancer, as well as on the development of rational strategies for drug discovery that targets epigenetic factors.

The formats for submissions include original research reports, reviews, perspectives/opinions, and methodology articles.

Prof. Dr. Pierre Olivier Angrand
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
  • epigenetic regulators
  • chromatin modifying enzymes
  • histone variants
  • non-coding RNAs
  • epigenetic therapy

Published Papers (2 papers)

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Research

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15 pages, 4651 KiB  
Article
CHST7 Methylation Status Related to the Proliferation and Differentiation of Pituitary Adenomas
by Wei Dong, Wenjian Shi, Yongliang Liu, Jingwu Li, Yu Zhang, Guilan Dong, Xiaoliu Dong and Hua Gao
Cells 2022, 11(15), 2400; https://doi.org/10.3390/cells11152400 - 04 Aug 2022
Cited by 3 | Viewed by 1864
Abstract
Pituitary adenomas (PAs) are the second most common primary brain tumor and may develop from any of the cell lineages responsible for producing the different pituitary hormones. DNA methylation is one of the essential epigenetic mechanisms in cancers, including PAs. In this study, [...] Read more.
Pituitary adenomas (PAs) are the second most common primary brain tumor and may develop from any of the cell lineages responsible for producing the different pituitary hormones. DNA methylation is one of the essential epigenetic mechanisms in cancers, including PAs. In this study, we measured the expression profile and promoter methylation status of carbohydrate sulfotransferase 7 (CHST7) in patients with PA; then, we investigated the effect of the CHST7 methylation status on the proliferation and differentiation of PAs. The volcano map and Metascape results showed that the levels of CHST7 were related to the lineages’ differentiation and the cell adhesion of PAs, and patients with low CHST7 had greater chances of having an SF-1 lineage (p = 0.002) and optic chiasm compression (p = 0.007). Reactome pathway analysis revealed that most of the DEGs involved in the regulation of TP53 regulated the transcription of cell cycle genes (HSA-6791312 and HSA6804116) in patients with high CHST7. Correlation analysis showed that CHST7 was significantly correlated with the eIF2/ATF4 pathway and mitochondrion-related genes. The AUC of ROC showed that CHST7 (0.288; 95% CI: 0.187–0.388) was superior to SF-1 (0.555; 95% CI: 0.440–0.671) and inferior to FSHB (0.804; 95% CI: 0.704–0.903) in forecasting the SF-1 lineage (p < 0.001). The SF-1 lineage showed a higher methylation frequency for CHST7 than the Pit-1 and TBX19 lineages (p = 0.009). Furthermore, as the key molecule of the hypothalamic–pituitary–gonadal axis, inhibin βE (INHBE) was positively correlated with the levels of CHST7 (r = 0.685, p < 0.001). In summary, CHST7 is a novel pituitary gland specific protein in SF-1 lineage adenomas with a potential role in gonadotroph cell proliferation and lineage differentiation in PAs. Full article
(This article belongs to the Special Issue Cancer Epigenetics: From Mechanism to Therapy)
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Review

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14 pages, 1553 KiB  
Review
The Role of N6-Methyladenosine in the Promotion of Hepatoblastoma: A Critical Review
by Finn Morgan Auld, Consolato M. Sergi, Roger Leng and Fan Shen
Cells 2022, 11(9), 1516; https://doi.org/10.3390/cells11091516 - 30 Apr 2022
Cited by 10 | Viewed by 2412
Abstract
Hepatoblastoma (HB) is a rare primary malignancy of the developing fetal liver. Its course is profoundly influenced by genetics, in the context of sporadic mutation or genetic syndromes. Conventionally, subtypes of HB are histologically determined based on the tissue type that is recapitulated [...] Read more.
Hepatoblastoma (HB) is a rare primary malignancy of the developing fetal liver. Its course is profoundly influenced by genetics, in the context of sporadic mutation or genetic syndromes. Conventionally, subtypes of HB are histologically determined based on the tissue type that is recapitulated by the tumor and the direction of its differentiation. This classification is being reevaluated based on advances on molecular pathology. The therapeutic approach comprises surgical intervention, chemotherapy (in a neoadjuvant or post-operative capacity), and in some cases, liver transplantation. Although diagnostic modalities and treatment options are evolving, some patients experience complications, including relapse, metastatic spread, and suboptimal response to chemotherapy. As yet, there is no consistent framework with which such outcomes can be predicted. N6-methyladenosine (m6A) is an RNA modification with rampant involvement in the normal processing of cell metabolism and neoplasia. It has been observed to impact the development of a variety of cancers via its governance of gene expression. M6A-associated genes appear prominently in HB. Literature data seem to underscore the role of m6A in promotion and clinical course of HB. Illuminating the pathogenetic mechanisms that drive HB are promising additions to the understanding of the clinically aggressive tumor behavior, given its potential to predict disease course and response to therapy. Implicated genes may also act as targets to facilitate the evolving personalized cancer therapy. Here, we explore the role of m6A and its genetic associates in the promotion of HB, and the impact this may have on the management of this neoplastic disease. Full article
(This article belongs to the Special Issue Cancer Epigenetics: From Mechanism to Therapy)
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