Special Issue "Mechanisms of Cell Death in Disease: A New Therapeutic Opportunity"

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (25 September 2019).

Special Issue Editors

Prof. Dr. Miguel Saceda Sanchez
E-Mail Website
Guest Editor
Institute of Research, Development and innovation in sanitary biotechnology of Elche (IDiBE)
Interests: Mechanisms of cell death; histone deacetylase inhibitor; cancer cells chemoresistance; cancer cells radioresistance; apoptosis; non-apoptotic cell death; pancreatic carcinoma; colon carcinoma; glioblastoma; signal transduction
Dr. Pilar Garcia-Morales
E-Mail Website
Co-Guest Editor
Institute of Research, Development and innovation in sanitary biotechnology of Elche (IDiBE)
Interests: Mechanisms of cell death; histone deacetylase inhibitor; cancer cells chemoresistance; cancer cells radioresistance; apoptosis; non-apoptotic cell death; pancreatic carcinoma; colon carcinoma; glioblastoma; signal transduction

Special Issue Information

Dear Colleagues,

The mechanisms involved in cell death have become an exciting research objective. There are many reasons for this interest. First, there is the clear relationship between cell death and disease, a relationship evident in all degenerative diseases—where different cellular processes lead to cell death in various tissues and organs and consequently to a loss of function—or alternatively to diseases that need to evade programmed cell death processes in order to achieve the progress of the disease, as is the case for autoimmune diseases or cancer. Second, additional interest arises from the need to develop new drugs capable of activating alternative cell death mechanisms in those diseases in which the traditional mechanisms of programmed cell death are totally or partially blocked. This search is particularly relevant in oncological diseases. Finally, there is an evident need for basic research into the mechanisms of cell death to clarify the different types and their regulation. We need to advance from exclusively considering classical apoptosis and necrosis as the only mechanisms of cell death, to talk about caspase-dependent or -independent programmed cell death, as well as talking about programmed necrosis, such as necroptosis. We must also face processes considered as cell survival, which under certain circumstances can mediate cell death, as is the case for autophagy. In this context, this Special Issue of Biomolecules seeks articles that will examine the mechanisms of cell death associated with the pathology of various types of diseases, from degenerative to oncological, as well as manuscripts that address the study of the mechanisms of action of the different drugs used to induce cell death in these diseases. Finally, articles that provide intimate knowledge of cell death mechanisms will be welcome.

Prof. Dr. Miguel Saceda Sanchez
Dr. Pilar Garcia-Morales
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 papers will be 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. Biomolecules 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 1200 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

  • Apoptotic cell death
  • Non-apoptotic cell death
  • Autophagy and cell death
  • Mechanisms of cell death as new therapeutic alternatives

Published Papers (2 papers)

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Research

Open AccessArticle
Characterization of the Anti-Cancer Activity of the Probiotic Bacterium Lactobacillus fermentum Using 2D vs. 3D Culture in Colorectal Cancer Cells
Biomolecules 2019, 9(10), 557; https://doi.org/10.3390/biom9100557 - 01 Oct 2019
Abstract
The aim of this study was to investigate the potential anti-cancer effects of probiotic cell-free supernatant (CFS) treatment using Lactobacillus fermentum for colorectal cancer (CRC) in 3D culture systems. Cell viability was assessed using MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt) assays, whereas apoptosis [...] Read more.
The aim of this study was to investigate the potential anti-cancer effects of probiotic cell-free supernatant (CFS) treatment using Lactobacillus fermentum for colorectal cancer (CRC) in 3D culture systems. Cell viability was assessed using MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt) assays, whereas apoptosis was monitored through RT-qPCR analysis of Bax, Bak, Noxa, and Bid mRNA expressions in addition to flow cytometry analysis of Lactobacillus cell-free supernatant (LCFS) treatment. Our results showed that the anti-cancer effect of LCFS on cell viability was pronouncedly enhanced in 3D-cultured HCT-116 cells, which was linked to the increased level of cleaved caspase 3. Additionally, upregulation of apoptotic marker gene mRNA transcription was dramatically increased in 3D cultured cells compared to 2D systems. In conclusion, this study suggests that LCFS enhances the activation of intrinsic apoptosis in HCT-116 cells and the potential anti-cancer effects of Lactobacilli mixtures in 3D culture systems. All in all, our study highlights the benefits of 3D culture models over 2D culture modeling in studying the anti-cancer effects of probiotics. Full article
(This article belongs to the Special Issue Mechanisms of Cell Death in Disease: A New Therapeutic Opportunity)
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Open AccessArticle
G-Protein-Coupled Estrogen Receptor (GPER)-Specific Agonist G1 Induces ER Stress Leading to Cell Death in MCF-7 Cells
Biomolecules 2019, 9(9), 503; https://doi.org/10.3390/biom9090503 - 18 Sep 2019
Abstract
The G-protein-coupled estrogen receptor (GPER) mediates rapid non-genomic effects of estrogen. Although GPER is able to induce proliferation, it is down-regulated in breast, ovarian and colorectal cancer. During cancer progression, high expression levels of GPER are favorable for patients’ survival. The GPER-specific agonist [...] Read more.
The G-protein-coupled estrogen receptor (GPER) mediates rapid non-genomic effects of estrogen. Although GPER is able to induce proliferation, it is down-regulated in breast, ovarian and colorectal cancer. During cancer progression, high expression levels of GPER are favorable for patients’ survival. The GPER-specific agonist G1 leads to an inhibition of cell proliferation and an elevated level of intracellular calcium (Ca2+). The purpose of this study is to elucidate the mechanism of G1-induced cell death by focusing on the connection between G1-induced Ca2+ depletion and endoplasmic reticulum (ER) stress in the estrogen receptor positive breast cancer cell line MCF-7. We found that G1-induced ER Ca2+ efflux led to the activation of the unfolded protein response (UPR), indicated by the phosphorylation of IRE1α and PERK and the cleavage of ATF6. The pro-survival UPR signaling was activated via up-regulation of the ER chaperon protein GRP78 and translational attenuation indicated by eIF2-α phosphorylation. However, the accompanying pro-death UPR signaling is profoundly activated and responsible for ER stress-induced cell death. Mechanistically, PERK-phosphorylation-induced JNK-phosphorylation and IRE1α-phosphorylation, which further triggered CAMKII-phosphorylation, are both implicated in G1-induced cell death. Our study indicates that loss of ER Ca2+ is responsible for G1-induced cell death via the pro-death UPR signaling. Full article
(This article belongs to the Special Issue Mechanisms of Cell Death in Disease: A New Therapeutic Opportunity)
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