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Mitophagy, Autophagy, Apoptosis and Senescence—the Roles of These Processes in...
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Mitophagy, Autophagy, Apoptosis and Senescence—the Roles of These Processes in Invasive Cancer Growth

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

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 7347

Special Issue Editors

Dr. Jozsef Dudas

E-Mail Website
Guest Editor
Department of Otorhinolaryngology, Medical University of Innsbruck, Innsbruck, Austria
Interests: epithelial-to-mesenchymal transition; fibroblasts; chemokines; head and neck squamous cell carcinoma; curcumin; tumor progression
Special Issues, Collections and Topics in MDPI journals
Dr. Mihaly Cserepes

E-Mail Website
Guest Editor
Department of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary
Interests: cancer metastasis; cancer cell biology; cancer therapy resistance; angiogenesis; tumor hypoxia

Special Issue Information

Dear Colleagues,

As global cancer incidence and fatality rates are increasing, more novel strategies are urgently needed to be involved in anticancer therapy regimens. As a well-known hallmark of cancer, cell death can be a cornerstone of effective treatment. However, in recent years, many distinct mechanisms and forms of cell death have been characterized, from regular apoptosis through autophagy to special events such as ferroptosis. These processes, on one hand, play a crucial role in cancer progression and therapy resistance, but on the other hand, they can also provide promising targets of novel treatment options.

In this Special Issue, we encourage submissions about the significance of alteration of cell death processes and senescence as a survival strategy of cancer cells, as well as any molecular background responsible for the different activity of these processes, and therapeutic approaches that induce cell death or target altered cell activities. 

Dr. Jozsef Dudas
Dr. Mihaly Cserepes
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

  • apoptosis
  • autophagy
  • mitophagy
  • senescence
  • cancer cell death mechanisms

Related Special Issue

Published Papers (4 papers)

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Research

14 pages, 4472 KiB  
Article
MET Oncogene Enhances Pro-Migratory Functions by Counteracting NMDAR2B Cleavage
by Simona Gallo, Annapia Vitacolonna, Paolo Maria Comoglio and Tiziana Crepaldi
Cells 2024, 13(1), 28; https://doi.org/10.3390/cells13010028 - 21 Dec 2023
Viewed by 864
Abstract
The involvement of the N-methyl-D-aspartate receptor (NMDAR), a glutamate-gated ion channel, in promoting the invasive growth of cancer cells is an area of ongoing investigation. Our previous findings revealed a physical interaction between NMDAR and MET, the hepatocyte growth factor (HGF) receptor. However, [...] Read more.
The involvement of the N-methyl-D-aspartate receptor (NMDAR), a glutamate-gated ion channel, in promoting the invasive growth of cancer cells is an area of ongoing investigation. Our previous findings revealed a physical interaction between NMDAR and MET, the hepatocyte growth factor (HGF) receptor. However, the molecular mechanisms underlying this NMDAR/MET interaction remain unclear. In this study, we demonstrate that the NMDAR2B subunit undergoes proteolytic processing, resulting in a low-molecular-weight form of 100 kDa. Interestingly, when the NMDAR2B and MET constructs were co-transfected, the full-size high-molecular-weight NMDAR2B form of 160 kDa was predominantly observed. The protection of NMDAR2B from cleavage was dependent on the kinase activity of MET. We provide the following evidence that MET opposes the autophagic lysosomal proteolysis of NMDAR2B: (i) MET decreased the protein levels of lysosomal cathepsins; (ii) treatment with either an inhibitor of autophagosome formation or the fusion of the autophagosome and lysosome elevated the proportion of the NMDAR2B protein’s uncleaved form; (iii) a specific mTOR inhibitor hindered the anti-autophagic effect of MET. Finally, we demonstrate that MET coopts NMDAR2B to augment cell migration. This implies that MET harnesses the functionality of NMDAR2B to enhance the ability of cancer cells to migrate. Full article
(This article belongs to the Special Issue Mitophagy, Autophagy, Apoptosis and Senescence—the Roles of These Processes in Invasive Cancer Growth)
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19 pages, 5052 KiB  
Article
Evolving Acquired Vemurafenib Resistance in a BRAF V600E Mutant Melanoma PDTX Model to Reveal New Potential Targets
by József Tóvári, Diána Vári-Mező, Sára Eszter Surguta, Andrea Ladányi, Attila Kigyós and Mihály Cserepes
Cells 2023, 12(14), 1919; https://doi.org/10.3390/cells12141919 - 24 Jul 2023
Cited by 2 | Viewed by 1530
Abstract
Malignant melanoma is challenging to treat, and metastatic cases need chemotherapy strategies. Targeted inhibition of commonly mutant BRAF V600E by inhibitors is efficient but eventually leads to resistance and progression in the vast majority of cases. Numerous studies investigated the mechanisms of resistance [...] Read more.
Malignant melanoma is challenging to treat, and metastatic cases need chemotherapy strategies. Targeted inhibition of commonly mutant BRAF V600E by inhibitors is efficient but eventually leads to resistance and progression in the vast majority of cases. Numerous studies investigated the mechanisms of resistance in melanoma cell lines, and an increasing number of in vivo or clinical data are accumulating. In most cases, bypassing BRAF and resulting reactivation of the MAPK signaling, as well as alternative PI3K-AKT signaling activation are reported. However, several unique changes were also shown. We developed and used a patient-derived tumor xenograft (PDTX) model to screen resistance evolution in mice in vivo, maintaining tumor heterogeneity. Our results showed no substantial activation of the canonical pathways; however, RNAseq and qPCR data revealed several altered genes, such as GPR39, CD27, SLC15A3, IFI27, PDGFA, and ABCB1. Surprisingly, p53 activity, leading to apoptotic cell death, was unchanged. The found biomarkers can confer resistance in a subset of melanoma patients via immune modulation, microenvironment changes, or drug elimination. Our resistance model can be further used in testing specific inhibitors that could be used in future drug development, and combination therapy testing that can overcome inhibitor resistance in melanoma. Full article
(This article belongs to the Special Issue Mitophagy, Autophagy, Apoptosis and Senescence—the Roles of These Processes in Invasive Cancer Growth)
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15 pages, 4460 KiB  
Article
C-MYC Inhibited Ferroptosis and Promoted Immune Evasion in Ovarian Cancer Cells through NCOA4 Mediated Ferritin Autophagy
by Yanping Jin, Jianping Qiu, Xiufang Lu and Guowei Li
Cells 2022, 11(24), 4127; https://doi.org/10.3390/cells11244127 - 19 Dec 2022
Cited by 23 | Viewed by 2823
Abstract
Objective: We aimed to construct the ferritin autophagy regulatory network and illustrate its mechanism in ferroptosis, TME immunity and malignant phenotypes of ovarian cancer. Methods: First, we used Western blot assays and immunohistochemistry to detect the pathway expression in ovarian cancer samples (C-MYC, [...] Read more.
Objective: We aimed to construct the ferritin autophagy regulatory network and illustrate its mechanism in ferroptosis, TME immunity and malignant phenotypes of ovarian cancer. Methods: First, we used Western blot assays and immunohistochemistry to detect the pathway expression in ovarian cancer samples (C-MYC, NCOA4). Then, we performed RIP and FISH analysis to verify the targeted binding of these factors after which we constructed ovarian cancer cell models and detected pathway regulator expression (NCOA4). Co-localization and Western blot assays were used to detect ferritin autophagy in different experimental groups. We selected corresponding kits to assess ROS contents in ovarian cancer cells. MMP was measured using flow cytometry and mitochondrial morphology was observed through TEM. Then, we chose Clone, EdU and Transwell to evaluate the proliferation and invasion abilities of ovarian cancer cells. We used Western blot assays to measure the DAMP content in ovarian cancer cell supernatants. Finally, we constructed tumor bearing models to study the effect of the C-MYC pathway on ovarian cancer tumorigenesis and TME immune infiltration in in vivo conditions. Results: Through pathway expression detection, we confirmed that C-MYC was obviously up-regulated and NCOA4 was obviously down-regulated in ovarian cancer samples, while their expression levels were closely related to the malignancy degree of ovarian cancer. RIP, FISH and cell model detection revealed that C-MYC could down-regulate NCOA4 expression through directly targeted binding with its mRNA. Ferritin autophagy and ferroptosis detection showed that C-MYC could inhibit ferroptosis through NCOA4-mediated ferritin autophagy, thus reducing ROS and inhibiting mitophagy in ovarian cancer cells. Cell function tests showed that C-MYC could promote the proliferation and invasion of ovarian cancer cells through the NCOA4 axis. The Western blot assay revealed that C-MYC could reduce HMGB1 release in ovarian cancer cells through the NCOA4 axis. In vivo experiments showed that C-MYC could promote tumorigenesis and immune evasion in ovarian cancer cells through inhibiting HMGB1 release induced by NCOA4-mediated ferroptosis. Conclusion: According to these results, we concluded that C-MYC could down-regulate NCOA4 expression through directly targeted binding, thus inhibiting ferroptosis and promoting malignant phenotype/immune evasion in ovarian cancer cells through inhibiting ferritin autophagy. Full article
(This article belongs to the Special Issue Mitophagy, Autophagy, Apoptosis and Senescence—the Roles of These Processes in Invasive Cancer Growth)
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14 pages, 3703 KiB  
Article
Comparison of Different Clinical Chemotherapeutical Agents’ Toxicity and Cell Response on Mesenchymal Stem Cells and Cancer Cells
by Flóra Vajda, Áron Szepesi, György Várady, Judit Sessler, Dániel Kiss, Zsuzsa Erdei, Kornélia Szebényi, Katalin Német, Gergely Szakács and András Füredi
Cells 2022, 11(19), 2942; https://doi.org/10.3390/cells11192942 - 20 Sep 2022
Viewed by 1623
Abstract
Mesenchymal stem cells (MSCs) or fibroblasts are one of the most abundant cell types in the tumor microenvironment (TME) exerting various anti- and pro-apoptotic effects during tumorigenesis, invasion, and drug treatment. Despite the recently discovered importance of MSCs in tumor progression and therapy, [...] Read more.
Mesenchymal stem cells (MSCs) or fibroblasts are one of the most abundant cell types in the tumor microenvironment (TME) exerting various anti- and pro-apoptotic effects during tumorigenesis, invasion, and drug treatment. Despite the recently discovered importance of MSCs in tumor progression and therapy, the response of these cells to chemotherapeutics compared to cancer cells is rarely investigated. A widely accepted view is that these naive MSCs have higher drug tolerance than cancer cells due to a significantly lower proliferation rate. Here, we examine the differences and similarities in the sensitivity of MSCs and cancer cells to nine diverse chemotherapy agents and show that, although MSCs have a slower cell cycle, these cells are still sensitive to various drugs. Surprisingly, MSCs showed similar sensitivity to a panel of compounds, however, suffered fewer DNA double-stranded breaks, did not enter into a senescent state, and was virtually incapable of apoptosis. Our results suggest that MSCs and cancer cells have different cell fates after drug treatment, and this could influence therapy outcome. These findings could help design drug combinations targeting both MSCs and cancer cells in the TME. Full article
(This article belongs to the Special Issue Mitophagy, Autophagy, Apoptosis and Senescence—the Roles of These Processes in Invasive Cancer Growth)
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