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Cells
Special Issues
Epigenetic Regulation of Cell Cycle and Cell Death in Pathogenesis
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Epigenetic Regulation of Cell Cycle and Cell Death in Pathogenesis

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 1269

Special Issue Editors

Dr. Vincenzo Carafa

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80138 Napoli, Italy
Interests: programmed cell death; apoptosis; leukaemia; epigenetic; acetylation; sirtuins
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Lucia Altucci

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80138 Napoli, Italy
Interests: leukaemia; epigenetic; personalized medicine; networking approaches
Special Issues, Collections and Topics in MDPI journals
Dr. Rosaria Benedetti

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80138 Napoli, Italy
Interests: solid cancer; cell signalling; drug resistance; methylation
Dr. Laura Della Torre

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80138 Napoli, Italy
Interests: cancer; regulated cell death; necroptosis

Special Issue Information

Dear Colleagues,

In multicellular organisms, cell proliferation and death are physiological events with a pivotal role in maintaining cellular homeostasis. During growth, cells undergo a high rate of proliferation both to increase in number and to complete the functionality of all components of the organism and have developed several processes to control the correct balance between the production of “new” cells and the elimination of “old” ones. Defects in intracellular signaling pathways related to cell proliferation and death, lead to altered protein function, which is responsible for the pathogenesis of several diseases such as cancer. 

Several studies have highlighted a direct link between epigenetic modifications and aberrant cell proliferation and death pathways. To this aim epigenetic modulator(s) can restore the altered or silenced cellular pathways, representing a promising tool for anticancer treatment.

Dr. Vincenzo Carafa
Prof. Dr. Lucia Altucci
Dr. Rosaria Benedetti
Dr. Laura Della Torre
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 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

  • cancer
  • cell proliferation
  • cell death
  • epigenetic

Published Papers (1 paper)

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Research

20 pages, 2761 KiB  
Article
ALKBH5 Stabilized N6-Methyladenosine—Modified LOC4191 to Suppress E. coli-Induced Apoptosis
by Haojun Xu, Changjie Lin, Chao Wang, Tianrui Zhao, Jinghan Yang, Junhao Zhang, Yanjun Hu, Xue Qi, Xi Chen, Yingyu Chen, Jianguo Chen, Aizhen Guo and Changmin Hu
Cells 2023, 12(22), 2604; https://doi.org/10.3390/cells12222604 - 10 Nov 2023
Viewed by 819
Abstract
E. coli is a ubiquitous pathogen that is responsible for over one million fatalities worldwide on an annual basis. In animals, E. coli can cause a variety of diseases, including mastitis in dairy cattle, which represents a potential public health hazard. However, the [...] Read more.
E. coli is a ubiquitous pathogen that is responsible for over one million fatalities worldwide on an annual basis. In animals, E. coli can cause a variety of diseases, including mastitis in dairy cattle, which represents a potential public health hazard. However, the pathophysiology of E. coli remains unclear. We found that E. coli could induce global upregulation of m6A methylation and cause serious apoptosis in bovine mammary epithelial cells (MAC-T cells). Furthermore, numerous m6A-modified lncRNAs were identified through MeRIP-seq. Interestingly, we found that the expression of LOC4191 with hypomethylation increased in MAC-T cells upon E. coli-induced apoptosis. Knocking down LOC4191 promoted E. coli-induced apoptosis and ROS levels through the caspase 3–PARP pathway. Meanwhile, knocking down ALKBH5 resulted in the promotion of apoptosis through upregulated ROS and arrested the cell cycle in MAC-T cells. ALKBH5 silencing accelerated LOC4191 decay by upregulating its m6A modification level, and the process was recognized by hnRNP A1. Therefore, this indicates that ALKBH5 stabilizes m6A-modified LOC4191 to suppress E. coli-induced apoptosis. This report discusses an initial investigation into the mechanism of m6A-modified lncRNA in cells under E. coli-induced apoptosis and provides novel insights into infectious diseases. Full article
(This article belongs to the Special Issue Epigenetic Regulation of Cell Cycle and Cell Death in Pathogenesis)
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