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5.2
3.9
Journals
Biomedicines
Special Issues
From DNA to mRNA Regulation of Autophagy
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From DNA to mRNA Regulation of Autophagy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 3523

Special Issue Editors

Dr. Michaël Guittaut

E-Mail Website
Guest Editor
INSERM, EFS BFC, UMR1098, RIGHT Institute, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, University Bourgogne Franche-Comté, 25000 Besançon, France
Interests: autophagy; gene regulation; epigenetics; NMD (nonsense-mediated mRNA decay); cancer; anti-tumor immunity
Dr. Aurélie Baguet

E-Mail Website
Guest Editor
INSERM, EFS BFC, UMR1098, RIGHT Institute, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, University Bourgogne Franche-Comté, 25000 Besançon, France
Interests: mRNA processing; gene expression regulation; NMD (nonsense-mediated mRNA decay); cancer

Special Issue Information

Dear Colleagues,

Autophagy, a protein degradation pathway, has attracted a strong interest over the last several decades because of its involvement in various human diseases—particularly in cancers. Nevertheless, even if the regulation of autophagy and its potential as a therapeutic target are the subjects of numerous studies, the resulting publications are mainly focused on the translational or post-translational regulation of autophagy. More recently, new mechanisms of gene regulation have emerged, such as post-transcriptional or epigenetic levels, and have been proposed to play an extensive role in the regulation of autophagy levels and flux.

This Issue therefore plans to attract interesting research projects studying the regulation of autophagy from the epigenetic control of expression of the ATG genes to the different aspects of mRNA metabolism as well as their protein expression. These new developing research areas might establish autophagy regulation as an interesting therapeutic target and lead, in the future, to the development of new anti-cancer treatments.

Dr. Michaël Guittaut
Dr. Aurélie Baguet
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • autophagy
  • cancer
  • epigenetics
  • RNA modifications (epitranscriptome)
  • mRNA metabolism (splicing, transport, modifications, partners, etc.)
  • mRNA stability and degradation (NMD, SMD, etc.)
  • translation and post-translational modifications

Published Papers (2 papers)

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Research

15 pages, 3766 KiB  
Article
Matrin3 (MATR3) Expression Is Associated with Hemophagocytosis
by Wen-Chi Yang, Sheng-Fung Lin, Shih-Chi Wu and Chih-Wen Shu
Biomedicines 2022, 10(9), 2161; https://doi.org/10.3390/biomedicines10092161 - 1 Sep 2022
Cited by 2 | Viewed by 1672
Abstract
Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome characterized by prolonged fever, cytopenia, hepatosplenomegaly, and hemophagocytosis. This occurs as a result of activated macrophages and impaired function of natural killer cells and/or cytotoxic T lymphocytes. The NF-κB pathway plays a crucial role in [...] Read more.
Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome characterized by prolonged fever, cytopenia, hepatosplenomegaly, and hemophagocytosis. This occurs as a result of activated macrophages and impaired function of natural killer cells and/or cytotoxic T lymphocytes. The NF-κB pathway plays a crucial role in hyperinflammation. Matrin3 (MATR3) is a nuclear RNA/DNA-binding protein that plays multiple roles in the regulation of gene expression. We enroll 62 patients diagnosed with secondary HLH and hemophagocytosis. Peripheral blood (PB) from 25 patients and 30 healthy volunteers and good quality bone marrow (BM) samples from 47 patients are collected and used for analysis. Clinical parameters, including age, sex, etiology, ferritin, fibrinogen, triglyceride, and viral infection status, had no association with survival prediction. Patients with downregulation of NF-κB and MATR3mRNA expression in the BM had a higher mortality rate. MATR3mRNA expression in PB was lower in patients compared to that in healthy volunteers. We use shRNA-MATR3-KD-THP1 cells to determine the efficacy of phagocytosis. We note that shRNA-MATR3-KD-THP1 cells had a higher phagocytic effect on necrotic Jurkat E6 cells and carboxylate modified polystyrene latex beads. Herein, we provide evidence of a new marker for clinical translation that can serve as a potential treatment target for secondary HLH. Full article
(This article belongs to the Special Issue From DNA to mRNA Regulation of Autophagy)
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10 pages, 1428 KiB  
Article
Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of Autophagy
by Kyung-Hyun Kim, Geum-Lan Hong, Yae-Ji Kim, Hui-Ju Lee and Ju-Young Jung
Biomedicines 2022, 10(8), 1981; https://doi.org/10.3390/biomedicines10081981 - 16 Aug 2022
Cited by 1 | Viewed by 1483
Abstract
Lethal giant larvae (Lgl) is an apical-basal polarity gene first identified in Drosophila. LLGL2 is one of the mammalian homologs of Lgl. However, little is known about its function in the prostate. In this study, to explore the new role of LLGL2 [...] Read more.
Lethal giant larvae (Lgl) is an apical-basal polarity gene first identified in Drosophila. LLGL2 is one of the mammalian homologs of Lgl. However, little is known about its function in the prostate. In this study, to explore the new role of LLGL2 in the prostate, we examined the proliferative activity of a BPH-1 cell line, a well-established model for the human prostate biology of benign prostatic hyperplasia (BPH). The expression of LLGL2 was dose-dependently increased in BPH-1 cells after treatment with 17β-estradiol (E2). Additionally, E2 treatment increased the proliferation of the BPH-1 cells. However, the knockdown of LLGL2 with siRNA significantly suppressed the proliferation of the E2-treated BPH-1 cells. Moreover, si-llgl2 treatment up-regulated the expression of LC-3B, ATG7, and p-beclin, which are known to play a pivotal role in autophagosome formation in E2-treated BPH-1 cells. Overexpression of LLGL2 was able to further prove these findings by showing the opposite results from the knockdown of LLGL2 in E2-treated BPH-1 cells. Collectively, our results suggest that LLGL2 is closely involved in the proliferation of prostate cells by regulating autophagosome formation. These results provide a better understanding of the mechanism involved in the effect of LLGL2 on prostate cell proliferation. LLGL2 might serve as a potential target in the diagnosis and/or treatment of human BPH. Full article
(This article belongs to the Special Issue From DNA to mRNA Regulation of Autophagy)
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