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Cells
Special Issues
Crosstalk of Autophagy and Apoptosis: Recent Advances
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Crosstalk of Autophagy and Apoptosis: Recent Advances

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (15 March 2025) | Viewed by 4027

Special Issue Editors

Prof. Dr. Maurizio Sorice

E-Mail Website
Guest Editor
Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena 324, 00161 Rome, Italy
Interests: autophagy; apoptosis; cell signaling; lipid rafts; lipid messengers; innate immunity; autoimmunity
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Valeria Manganelli

E-Mail Website
Guest Editor
Department of Experimental Medicine, Sapienza University of Rome, viale Regina Elena 324, 00161 Rome, Italy
Interests: autophagy; apoptosis; cell signaling; lipid rafts; lipid messengers; HMGB1; cancer

Special Issue Information

Dear Colleagues,

Autophagy and apoptosis represent two fundamental pathophysiological mechanisms of cell fate regulation. However, the signaling pathways of both of these processes are significantly interconnected through various mechanisms of crosstalk.

Recent studies further clarified the molecules and signaling pathways involved in this crosstalk, involving both proteins and lipids. In this regard, mitochondria-associated membranes (MAMs) have been identified as critical hubs in the regulation of apoptosis, autophagy, and tumor growth. Recently, lipid rafts, which have been detected within MAMs, were shown to represent a physical and functional platform, operating during the early steps of the autophagic process.

The purpose of this Special Issue is to outline the more recent knowledge on the signal transduction pathways involved in the autophagy/apoptosis crosstalk and investigate the bioactive properties of drugs with antitumor activities, focusing on their role in the regulation of autophagy and cell death crosstalk that triggers the uncontrolled expansion of tumor cells. Furthermore, autophagy has emerged as a key mechanism in the survival and function of T and B lymphocytes, and its activation is involved in apoptotic resistance in autoimmune diseases. An additional purpose of this Special Issue is to investigate whether the relationship between autophagy and apoptosis impacts the response to the therapy.

Understanding the molecular pathways involved in the apoptosis–autophagy relationship is a fundamental step in the knowledge of mechanisms regulating cell death and survival. This understanding may drive the development of new therapeutic strategies for cancer and/or autoimmune diseases.

Prof. Dr. Maurizio Sorice
Prof. Dr. Valeria Manganelli
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

  • autophagy 
  • apoptosis 
  • cell signaling 
  • mitochondria 
  • MAMs 
  • lipid rafts 
  • cancer therapy 
  • autoimmunity

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Related Special Issue

Published Papers (3 papers)

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Research

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23 pages, 1754 KiB  
Article
Genomic and Phenotypic Characterization of CHO 4BGD Cells with Quad Knockout and Overexpression of Two Housekeeping Genes That Allow for Metabolic Selection and Extended Fed-Batch Culturing
by Nadezhda Alexandrovna Orlova, Maria Valerievna Sinegubova, Denis Eduardovich Kolesov, Yulia Alexandrovna Khodak, Victor Vyacheslavovich Tatarskiy and Ivan Ivanovich Vorobiev
Cells 2025, 14(10), 692; https://doi.org/10.3390/cells14100692 - 11 May 2025
Viewed by 1163
Abstract
Re-engineering of CHO cells using genome editing and the overexpression of multiple helper genes is the central track for obtaining better cell lines for the production of biopharmaceuticals. Using two subsequent rounds of genome editing of the CHO S cells, we have developed [...] Read more.
Re-engineering of CHO cells using genome editing and the overexpression of multiple helper genes is the central track for obtaining better cell lines for the production of biopharmaceuticals. Using two subsequent rounds of genome editing of the CHO S cells, we have developed the cell line CHO 4BGD with four knockouts of two pro-apoptotic genes bak1 and bax, and two common selection markers genes—glul (GS) and dhfr, and additional copies of genes bcl-2 and beclin-1 used for enhancement of macroautophagy. The NGS sequencing of 4BGD cells revealed that all eight targeted alleles were successfully disrupted. Two edited loci out of eight contained large inserts of non-relevant DNA. Further data analysis shows that cells have no off-target DNA editing events, and all known CHO genes are preserved. The cells obtained are completely resistant to the induction of apoptosis, and they are suitable for the generation of stably transfected cell lines with the dhfr selection marker. They also properly undergo the target gene amplification. The 4BGD-derived clonal cell line that secretes the monoclonal antibody retains the ability for prolonged fed-batch culturing. The method of obtaining multiply edited CHO cells using the multiplex CRISPR/Cas9 editing and simultaneous stable transfection of plasmids, coding for the housekeeping genes, is suitable for the rapid generation of massively edited CHO cells. Full article
(This article belongs to the Special Issue Crosstalk of Autophagy and Apoptosis: Recent Advances)
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18 pages, 4607 KiB  
Article
Inhibition of Autophagy by Berbamine Hydrochloride Mitigates Tumor Immune Escape by Elevating MHC-I in Melanoma Cells
by Jinhuan Xian, Leilei Gao, Zhenyang Ren, Yanjun Jiang, Junjun Pan, Zheng Ying, Zhenyuan Guo, Qingsong Du, Xu Zhao, He Jin, Hua Yi, Jieying Guan and Shan Hu
Cells 2024, 13(18), 1537; https://doi.org/10.3390/cells13181537 - 13 Sep 2024
Cited by 5 | Viewed by 1453
Abstract
Impaired tumor cell antigen presentation contributes significantly to immune evasion. This study identifies Berbamine hydrochloride (Ber), a compound derived from traditional Chinese medicine, as an effective inhibitor of autophagy that enhances antigen presentation in tumor cells. Ber increases MHC-I-mediated antigen presentation in melanoma [...] Read more.
Impaired tumor cell antigen presentation contributes significantly to immune evasion. This study identifies Berbamine hydrochloride (Ber), a compound derived from traditional Chinese medicine, as an effective inhibitor of autophagy that enhances antigen presentation in tumor cells. Ber increases MHC-I-mediated antigen presentation in melanoma cells, improving recognition and elimination by CD8+ T cells. Mutation of Atg4b, which blocks autophagy, also raises MHC-I levels on the cell surface, and further treatment with Ber under these conditions does not increase MHC-I, indicating Ber’s role in blocking autophagy to enhance MHC-I expression. Additionally, Ber treatment leads to the accumulation of autophagosomes, with elevated levels of LC3-II and p62, suggesting a disrupted autophagic flux. Fluorescence staining and co-localization analyses reveal that Ber likely inhibits lysosomal acidification without hindering autophagosome–lysosome fusion. Importantly, Ber treatment suppresses melanoma growth in mice and enhances CD8+ T cell infiltration, supporting its therapeutic potential. Our findings demonstrate that Ber disturbs late-stage autophagic flux through abnormal lysosomal acidification, enhancing MHC-I-mediated antigen presentation and curtailing tumor immune escape. Full article
(This article belongs to the Special Issue Crosstalk of Autophagy and Apoptosis: Recent Advances)
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Review

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27 pages, 2016 KiB  
Review
Extracellular Vesicles in the Crosstalk of Autophagy and Apoptosis: A Role for Lipid Rafts
by Agostina Longo, Valeria Manganelli, Roberta Misasi, Gloria Riitano, Tuba Rana Caglar, Elena Fasciolo, Serena Recalchi, Maurizio Sorice and Tina Garofalo
Cells 2025, 14(10), 749; https://doi.org/10.3390/cells14100749 - 20 May 2025
Viewed by 584
Abstract
Autophagy and apoptosis are two essential mechanisms regulating cell fate. Although distinct, their signaling pathways are closely interconnected through various crosstalk mechanisms. Lipid rafts are described to act as both physical and functional platforms during the early stages of autophagic and apoptotic processes. [...] Read more.
Autophagy and apoptosis are two essential mechanisms regulating cell fate. Although distinct, their signaling pathways are closely interconnected through various crosstalk mechanisms. Lipid rafts are described to act as both physical and functional platforms during the early stages of autophagic and apoptotic processes. Only recently has a role for lipid raft-associated molecules in regulating EV biogenesis and release begun to emerge. In particular, lipids of EV membranes are essential components in conferring stability to these vesicles in different extracellular environments and/or to facilitate binding or uptake into recipient cells. In this review we highlight these aspects, focusing on the role of lipid molecules during apoptosis and secretory autophagy pathways. We describe the molecular machinery that connects autophagy and apoptosis with vesicular trafficking and lipid metabolism during the release of EVs, and how their alterations contribute to the development of various diseases, including autoimmune disorders and cancer. Overall, these findings emphasize the complexity of autophagy/apoptosis crosstalk and its key role in cellular dynamics, supporting the role of lipid rafts as new therapeutic targets. Full article
(This article belongs to the Special Issue Crosstalk of Autophagy and Apoptosis: Recent Advances)
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