Emerging Insights into Cell Death in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (25 October 2024) | Viewed by 3213

Special Issue Editor


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Guest Editor
Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80138 Napoli, Italy
Interests: programmed cell death; apoptosis; leukaemia; epigenetic; acetylation; sirtuins
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Special Issue Information

Dear Colleagues,

We are thrilled to announce a Special Issue entitled "Emerging Insights into Cell Death in Cancer" that delves into the intricate relationship between cell death pathways and cancer, building upon the foundational understanding laid out in the previous Special Issue, "Deregulation of Cell Death in Cancer". The delicate balance between cell proliferation and elimination is central to the maintenance of biological homeostasis, and disruptions to this equilibrium can lead to various pathologies, including cancer.

One of the key hallmarks of cancer is the evasion of apoptosis, a highly orchestrated programmed cell death process characterized by distinct cellular events such as membrane disruption, DNA fragmentation, and cellular debris removal. Understanding the molecular mechanisms underlying regulated cell death (RCD) is crucial for unraveling the complexities of cancer initiation, progression, and metastasis.

Recent advancements have led to the identification and classification of different forms of RCD, shedding light on novel targets and pathways for therapeutic intervention. Given the limitations of conventional diagnostic methods for early-stage cancer detection and the observed treatment resistance associated with apoptotic pathway dysregulation, there is a pressing need to explore the modulation and restoration of RCD equilibrium as a promising avenue for anticancer therapy.

This Special Issue aims to showcase cutting-edge research elucidating the interplay between cancer and RCD, offering fresh insights into cellular mechanisms, drug discovery, and therapeutic strategies centered around apoptosis. By delving deeper into the role of RCD in carcinogenesis, this collection of articles seeks to advance our understanding and pave the way for more effective cancer treatments.

We invite researchers, academicians, and practitioners to contribute original research articles, reviews, and communications that advance our understanding of regulated cancer death and its role in cancer.

Dr. Vincenzo Carafa
Guest Editor

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Keywords

  • cell death
  • cancer
  • apoptosis
  • programmed cell death (PCD)
  • regulated cell death (RCD)
  • therapeutic strategies
  • molecular mechanisms
  • drug discovery
  • cellular pathways
  • biomarkers
  • immunotherapy
  • targeted therapy
  • cellular signaling
  • apoptotic regulators

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Published Papers (3 papers)

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Research

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26 pages, 6512 KiB  
Article
p66Shc Protein—Oxidative Stress Sensor or Redox Enzyme: Its Potential Role in Mitochondrial Metabolism of Human Breast Cancer
by Monika Prill, Vilma A. Sardão, Mateusz Sobczak, Dominika Nowis, Jedrzej Szymanski and Mariusz R. Wieckowski
Cancers 2024, 16(19), 3324; https://doi.org/10.3390/cancers16193324 - 28 Sep 2024
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Abstract
This work presents a comprehensive evaluation of the role of p66Shc protein in mitochondrial physiology in MDA-MB-231 breast cancer cells. The use of human breast cancer cell line MDA-MB-231 and its genetically modified clones (obtained with the use of the CRISPR-Cas9 technique), expressing [...] Read more.
This work presents a comprehensive evaluation of the role of p66Shc protein in mitochondrial physiology in MDA-MB-231 breast cancer cells. The use of human breast cancer cell line MDA-MB-231 and its genetically modified clones (obtained with the use of the CRISPR-Cas9 technique), expressing different levels of p66Shc protein, allowed us to demonstrate how the p66Shc protein affects mitochondrial metabolism of human breast cancer cells. Changes in the level of p66Shc (its overexpression, and overexpressing of its Serine 36-mutated version, as well as the knockout of p66Shc) exert different effects in breast cancer cells. Interestingly, knocking out p66Shc caused significant changes observed mostly in mitochondrial bioenergetic parameters. We have shown that an MDA-MB-231 (which is a strong metastatic type of breast cancer) clone lacking p66Shc protein is characterized by a significant shift in the metabolic phenotype in comparison to other MDA-MB-231 clones. Additionally, this clone is significantly more vulnerable to doxorubicin treatment. We have proved that p66Shc adaptor protein in human breast cancer cells may exert a different role than in noncancerous cells (e.g., fibroblasts). Full article
(This article belongs to the Special Issue Emerging Insights into Cell Death in Cancer)
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20 pages, 6055 KiB  
Article
Anticancer Activity of Delta-Tocotrienol in Human Hepatocarcinoma: Involvement of Autophagy Induction
by Marina Montagnani Marelli, Chiara Macchi, Massimiliano Ruscica, Patrizia Sartori and Roberta Manuela Moretti
Cancers 2024, 16(15), 2654; https://doi.org/10.3390/cancers16152654 - 26 Jul 2024
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Abstract
(1) Hepatocellular carcinoma (HCC) is the predominant form of primary liver cancer. Surgical resection, tumor ablation, and liver transplantation are curative treatments indicated for early-stage HCC. The management of intermediate and advanced stages of pathology is based on the use of systemic therapies [...] Read more.
(1) Hepatocellular carcinoma (HCC) is the predominant form of primary liver cancer. Surgical resection, tumor ablation, and liver transplantation are curative treatments indicated for early-stage HCC. The management of intermediate and advanced stages of pathology is based on the use of systemic therapies which often show important side effects. Vitamin E-derivative tocotrienols (TTs) play antitumoral properties in different tumors. Here, we analyzed the activity of delta-TT (δ-TT) on HCC human cell lines. (2) We analyzed the ability of δ-TT to trigger apoptosis, to induce oxidative stress, autophagy, and mitophagy in HepG2 cell line. We evaluated the correlation between the activation of autophagy with the ability of δ-TT to induce cell death. (3) The data obtained demonstrate that δ-TT exerts an antiproliferative and proapoptotic effect in HCC cells. Furthermore, δ-TT induces the release of mitochondrial ROS and causes a structural and functional alteration of the mitochondria compatible with a fission process. Finally, δ-TT triggers selective autophagy process removing dysfunctional mitochondria. Inhibition of autophagy reversed the cytotoxic action of δ-TT. (4) Our results demonstrate that δ-TT through the activation of autophagy could represent a potential new approach in the treatment of advanced HCC. Full article
(This article belongs to the Special Issue Emerging Insights into Cell Death in Cancer)
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Review

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29 pages, 1077 KiB  
Review
Deregulation of New Cell Death Mechanisms in Leukemia
by Gregorio Favale, Federica Donnarumma, Vincenza Capone, Laura Della Torre, Antonio Beato, Daniela Carannante, Giulia Verrilli, Asmat Nawaz, Francesco Grimaldi, Maria Carla De Simone, Nunzio Del Gaudio, Wouter Leonard Megchelenbrink, Michele Caraglia, Rosaria Benedetti, Lucia Altucci and Vincenzo Carafa
Cancers 2024, 16(9), 1657; https://doi.org/10.3390/cancers16091657 - 25 Apr 2024
Cited by 1 | Viewed by 1295
Abstract
Hematological malignancies are among the top five most frequent forms of cancer in developed countries worldwide. Although the new therapeutic approaches have improved the quality and the life expectancy of patients, the high rate of recurrence and drug resistance are the main issues [...] Read more.
Hematological malignancies are among the top five most frequent forms of cancer in developed countries worldwide. Although the new therapeutic approaches have improved the quality and the life expectancy of patients, the high rate of recurrence and drug resistance are the main issues for counteracting blood disorders. Chemotherapy-resistant leukemic clones activate molecular processes for biological survival, preventing the activation of regulated cell death pathways, leading to cancer progression. In the past decade, leukemia research has predominantly centered around modulating the well-established processes of apoptosis (type I cell death) and autophagy (type II cell death). However, the development of therapy resistance and the adaptive nature of leukemic clones have rendered targeting these cell death pathways ineffective. The identification of novel cell death mechanisms, as categorized by the Nomenclature Committee on Cell Death (NCCD), has provided researchers with new tools to overcome survival mechanisms and activate alternative molecular pathways. This review aims to synthesize information on these recently discovered RCD mechanisms in the major types of leukemia, providing researchers with a comprehensive overview of cell death and its modulation. Full article
(This article belongs to the Special Issue Emerging Insights into Cell Death in Cancer)
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