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Apoptosis and Autophagy as Strategies in Cancer Treatment

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 March 2025 | Viewed by 2819

Special Issue Editor


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Guest Editor
Medical College, Jagiellonian University, Chair of Medical Biochemistry, Ul. Kopernika 7, 31-034 Kraków, Poland
Interests: apoptosis; autophagy; cancer therapy treatment; drug resistance

Special Issue Information

Dear Colleagues,

Apoptosis and autophagy, two pathways involved in cell death, are extensive areas of research in the context of anticancer therapies. Both of these processes play a key role in maintaining homeostasis and participate in pathological processes related to carcinogenesis.

Apoptosis, a type of programmed cell death, is often suppressed in cancer cells and is considered a hallmark of cancer development.

Autophagy is a basic cellular mechanism occurring in every living cell, involving the digestion of cytoplasm fragments or entire cell organelles to obtain an endogenous energy source. It is associated with many intracellular signaling pathways, in particular nutrient-sensing mechanisms and cell-death-signaling cascades. The role of autophagy in cancer may be different; this process can not only activate and inhibit cell death but also facilitate switching between cell death mechanisms.

This Special Issue aims to present the latest original research and reviews on the modulation of the processes of apoptosis and autophagy in anticancer treatments. I hope that the latest research results presented in this Special Issue will contribute to a more profound understanding of the processes related to cell death and will be helpful in anticancer therapies.

Dr. Dorota Ciołczyk-Wierzbicka 
Guest Editor

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Keywords

  • apoptosis
  • autophagy
  • cancer therapy/treatment
  • drug resistance
  • signaling pathways

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Published Papers (2 papers)

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Research

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34 pages, 23510 KiB  
Article
Di- and Triselenoesters—Promising Drug Candidates for the Future Therapy of Triple-Negative Breast Cancer
by Dominika Radomska, Robert Czarnomysy, Anna Szymanowska, Dominik Radomski, Magda Chalecka, Arkadiusz Surazynski, Enrique Domínguez-Álvarez, Anna Bielawska and Krzysztof Bielawski
Int. J. Mol. Sci. 2024, 25(14), 7764; https://doi.org/10.3390/ijms25147764 - 16 Jul 2024
Cited by 1 | Viewed by 835
Abstract
Breast cancer is a major malignancy among women, characterized by a high mortality rate. The available literature evidence indicates that selenium, as a trace element, has chemopreventive properties against many types of cancer; as such, compounds containing it in their structure may potentially [...] Read more.
Breast cancer is a major malignancy among women, characterized by a high mortality rate. The available literature evidence indicates that selenium, as a trace element, has chemopreventive properties against many types of cancer; as such, compounds containing it in their structure may potentially exhibit anticancer activity. Accordingly, we have undertaken a study to evaluate the effects of novel selenoesters (EDAG-1, -7, -8, -10) on MCF-7 and MDA-MB-231 breast cancer cells. Our analysis included investigations of cell proliferation and viability as well as cytometric determinations of apoptosis/autophagy induction, changes in mitochondrial membrane polarity (ΔΨm), caspase 3/7, 8, and 9 activities, and Bax, Bcl-2, p53, Akt, AMPK, and LC3A/B proteins. The obtained data revealed that the tested derivatives are highly cytotoxic and inhibit cell proliferation even at nanomolar doses (0.41–0.79 µM). Importantly, their strong proapoptotic properties (↑ caspase 3/7) are attributable to the effects on both the extrinsic (↑ caspase 8) and intrinsic (↓ ΔΨm and Bcl-2, ↑ Bax, p53, and caspase 9) pathways of apoptosis. Moreover, the tested compounds are autophagy activators (↓ Akt, ↑ autophagosomes and autolysosomes, AMPK, LC3A/B). In summary, the potent anticancer activity suggests that the tested compounds may be promising drug candidates for future breast cancer therapy. Full article
(This article belongs to the Special Issue Apoptosis and Autophagy as Strategies in Cancer Treatment)
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Review

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18 pages, 984 KiB  
Review
Decoding the Versatile Landscape of Autophagic Protein VMP1 in Cancer: A Comprehensive Review across Tissue Types and Regulatory Mechanisms
by Felipe J. Renna, Claudio D. Gonzalez and Maria I. Vaccaro
Int. J. Mol. Sci. 2024, 25(7), 3758; https://doi.org/10.3390/ijms25073758 - 28 Mar 2024
Cited by 2 | Viewed by 1663
Abstract
Autophagy, a catabolic process orchestrating the degradation of proteins and organelles within lysosomes, is pivotal for maintaining cellular homeostasis. However, its dual role in cancer involves preventing malignant transformation while fostering progression and therapy resistance. Vacuole Membrane Protein 1 (VMP1) is an essential [...] Read more.
Autophagy, a catabolic process orchestrating the degradation of proteins and organelles within lysosomes, is pivotal for maintaining cellular homeostasis. However, its dual role in cancer involves preventing malignant transformation while fostering progression and therapy resistance. Vacuole Membrane Protein 1 (VMP1) is an essential autophagic protein whose expression, per se, triggers autophagy, being present in the whole autophagic flux. In pancreatic cancer, VMP1—whose expression is linked to the Kirsten Rat Sarcoma Virus (KRAS) oncogene—significantly contributes to disease promotion, progression, and chemotherapy resistance. This investigation extends to breast cancer, colon cancer, hepatocellular carcinoma, and more, highlighting VMP1’s nuanced nature, contingent on specific tissue contexts. The examination of VMP1’s interactions with micro-ribonucleic acids (miRNAs), including miR-21, miR-210, and miR-124, enhances our understanding of its regulatory network in cancer. Additionally, this article discusses VMP1 gene fusions, especially with ribosomal protein S6 kinase B1 (RPS6KB1), shedding light on potential implications for tumor malignancy. By deciphering the molecular mechanisms linking VMP1 to cancer progression, this exploration paves the way for innovative therapeutic strategies to disrupt these pathways and potentially improve treatment outcomes. Full article
(This article belongs to the Special Issue Apoptosis and Autophagy as Strategies in Cancer Treatment)
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