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

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

Deadline for manuscript submissions: closed (20 October 2024) | Viewed by 1522

Special Issue Editors


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Guest Editor
Department of Otorhinolaryngology, Medical University of Innsbruck, Innsbruck, Austria
Interests: clinical cancer; head and neck oncology; miRNA and exosomes; tumor microenvironment; 2D and 3D cell culture; experimental photodynamic therapy; image cytometry

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
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Special Issue Information

Dear Colleagues,

As global cancer incidence and fatality rates increase, more novel strategies are urgently needed for 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 the one hand, play a crucial role in cancer progression and therapy resistance; however, on the other hand, they can also provide promising targets of novel treatment options.

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

Dr. Julia Federspiel
Dr. Jozsef Dudas
Guest Editors

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Keywords

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

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Research

13 pages, 9327 KiB  
Article
BCL-B Promotes Lung Cancer Invasiveness by Direct Inhibition of BOK
by Palaniappan Ramesh, Amal R. Al Kadi, Gaurav M. Borse, Maximilian Webendörfer, Gregor Zaun, Martin Metzenmacher, Fabian Doerr, Servet Bölükbas, Balazs Hegedüs, Smiths S. Lueong, Joelle Magne, Beiyun Liu, Greisly Nunez, Martin Schuler, Douglas R. Green and Halime Kalkavan
Cells 2025, 14(4), 246; https://doi.org/10.3390/cells14040246 - 9 Feb 2025
Viewed by 1118
Abstract
Expression of BCL-B, an anti-apoptotic BCL-2 family member, is correlated with worse survival in lung adenocarcinomas. Here, we show that BCL-B can mitigate cell death initiation through interaction with the effector protein BOK. We found that this interaction can promote sublethal mitochondrial [...] Read more.
Expression of BCL-B, an anti-apoptotic BCL-2 family member, is correlated with worse survival in lung adenocarcinomas. Here, we show that BCL-B can mitigate cell death initiation through interaction with the effector protein BOK. We found that this interaction can promote sublethal mitochondrial outer membrane permeabilization (MOMP) and consequently generate apoptosis-flatliners, which represent a source of drug-tolerant persister cells (DTPs). The engagement of endothelial-mesenchymal-transition (EMT) further promotes cancer cell invasiveness in such DTPs. Our results reveal that BCL-B fosters cancer cell aggressiveness by counteracting complete MOMP. Full article
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