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: 15 March 2025 | Viewed by 1430

Special Issue Editors


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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

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

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Keywords

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

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Published Papers (1 paper)

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Research

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
Viewed by 889
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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