Mechanisms of Cell Death in Cancer Cells: A New Therapeutic Opportunity—2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 4325

Special Issue Editor


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Guest Editor
MedFuture Research Center for Advanced Medicine, “Iuliu Hațieganu” University of Medicine and Pharmacy, 400377 Cluj-Napoca, Romania
Interests: signaling pathways; biochemistry; cell-culture; cell death mechanism; cancer research; hematology
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Special Issue Information

Dear Colleagues,

Cancer initiation and progression are driven by a complex interplay of genetic errors, environmental factors, and dysregulated molecular pathways. Among these pathways, the mechanism of cell death plays a critical role in regulating tumor growth and survival. Alterations in cell death pathways enable cancer cells to evade apoptosis, proliferate uncontrollably, and resist therapy. Therefore, targeting these pathways represents a promising therapeutic strategy for combating cancer.

This Special Issue aims to showcase cutting-edge research focused on elucidating the molecular mechanisms underlying cell death dysregulation in cancer and identifying novel therapeutic compounds capable of restoring its normal function. The featured studies will highlight both newly discovered molecules and repurposed drugs, offering insights into innovative strategies for overcoming treatment resistance and improving patient outcomes in both solid tumors and hematological malignancies.

The research presented in this collection will delve into the intricate molecular events driving cell death dysregulation in cancer, including disruptions in signaling cascades, DNA repair mechanisms, and the aberrant expression of regulatory proteins. Furthermore, the impact of environmental factors such as carcinogen exposure and chronic inflammation on these processes will be explored. By unraveling the complex mechanisms governing cell death in cancer, researchers aim to identify vulnerabilities that can be exploited for therapeutic intervention.

Through comprehensive exploration of the cell death machinery, this Special Issue seeks to accelerate the development of effective anti-cancer therapies with broad applicability across diverse cancer types. By highlighting promising compounds and therapeutic approaches, the collection aims to provide valuable insights into the future of cancer treatment and pave the way for improved outcomes for patients worldwide.

Dr. Adrian-Bogdan Țigu
Guest Editor

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Keywords

  • cell death
  • drug repositioning
  • translational research
  • oncology
  • cancer therapy
  • apoptosis

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Related Special Issue

Published Papers (3 papers)

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Research

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20 pages, 7679 KiB  
Article
Parecoxib and 5-Fluorouracil Synergistically Inhibit EMT and Subsequent Metastasis in Colorectal Cancer by Targeting PI3K/Akt/NF-κB Signaling
by Wan-Ling Chang, Jyun-Yu Peng, Chain-Lang Hong, Pei-Ching Li, Fung-Jou Lu and Ching-Hsein Chen
Biomedicines 2024, 12(7), 1526; https://doi.org/10.3390/biomedicines12071526 - 9 Jul 2024
Cited by 1 | Viewed by 1013
Abstract
Colorectal cancer is one of the most common causes of cancer mortality worldwide, and innovative drugs for the treatment of colorectal cancer are continually being developed. 5-Fluorouracil (5-FU) is a common clinical chemotherapeutic drug. Acquired resistance to 5-FU is a clinical challenge in [...] Read more.
Colorectal cancer is one of the most common causes of cancer mortality worldwide, and innovative drugs for the treatment of colorectal cancer are continually being developed. 5-Fluorouracil (5-FU) is a common clinical chemotherapeutic drug. Acquired resistance to 5-FU is a clinical challenge in colorectal cancer treatment. Parecoxib is a selective COX-2-specific inhibitor that was demonstrated to inhibit metastasis in colorectal cancers in our previous study. This study aimed to investigate the synergistic antimetastatic activities of parecoxib to 5-FU in human colorectal cancer cells and determine the underlying mechanisms. Parecoxib and 5-FU synergistically suppressed metastasis in colorectal cancer cells. Treatment with the parecoxib/5-FU combination induced an increase in E-cadherin and decrease in β-catenin expression. The parecoxib/5-FU combination inhibited MMP-9 activity, and the NF-κB pathway was suppressed as well. Mechanistic analysis denoted that the parecoxib/5-FU combination hindered the essential molecules of the PI3K/Akt route to obstruct metastatic colorectal cancer. Furthermore, the parecoxib/5-FU combination could inhibit reactive oxygen species. Our work showed the antimetastatic capacity of the parecoxib/5-FU combination for treating colorectal cancers via the targeting of the PI3K/Akt/NF-κB pathway. Full article
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16 pages, 2831 KiB  
Review
Review of T Helper 2-Type Inflammatory Diseases Following Immune Checkpoint Inhibitor Treatment
by Yoshihito Mima, Tsutomu Ohtsuka, Ippei Ebato, Yukihiro Nakata, Akihiro Tsujita, Yoshimasa Nakazato and Yuta Norimatsu
Biomedicines 2024, 12(8), 1886; https://doi.org/10.3390/biomedicines12081886 - 19 Aug 2024
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Abstract
Immune checkpoints are mechanisms that allow cancer cells to evade immune surveillance and avoid destruction by the body’s immune system. Tumor cells exploit immune checkpoint proteins to inhibit T cell activation, thus enhancing their resistance to immune attacks. Immune checkpoint inhibitors, like nivolumab, [...] Read more.
Immune checkpoints are mechanisms that allow cancer cells to evade immune surveillance and avoid destruction by the body’s immune system. Tumor cells exploit immune checkpoint proteins to inhibit T cell activation, thus enhancing their resistance to immune attacks. Immune checkpoint inhibitors, like nivolumab, work by reactivating these suppressed T cells to target cancer cells. However, this reactivation can disrupt immune balance and cause immune-related adverse events. This report presents a rare case of prurigo nodularis that developed six months after administering nivolumab for lung adenocarcinoma. While immune-related adverse events are commonly linked to T helper-1- or T helper-17-type inflammations, T helper-2-type inflammatory reactions, as observed in our case, are unusual. The PD-1–PD-L1 pathway is typically associated with T helper-1 and 17 responses, whereas the PD-1–PD-L2 pathway is linked to T helper-2 responses. Inhibition of PD-1 can enhance PD-L1 functions, potentially shifting the immune response towards T helper-1 and 17 types, but it may also influence T helper-2-type inflammation. This study reviews T helper-2-type inflammatory diseases emerging from immune checkpoint inhibitor treatment, highlighting the novelty of our findings. Full article
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17 pages, 1657 KiB  
Review
Advanced and Metastatic Non-Melanoma Skin Cancer: Epidemiology, Risk Factors, Clinical Features, and Treatment Options
by Zoe Gabrielle Attal, Walid Shalata, Arina Soklakova, Lena Tourkey, Sondos Shalata, Omar Abu Saleh, Fahed Abu Salamah, Ibrahim Alatawneh and Alexander Yakobson
Biomedicines 2024, 12(7), 1448; https://doi.org/10.3390/biomedicines12071448 - 28 Jun 2024
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Abstract
Non-melanoma skin cancers (NMSC) form the majority of skin cancers, with basal cell carcinoma (BCC) being the most common and cutaneous squamous cell carcinoma (cSCC) being second. Prolonged ultraviolet (UV) exposure, aging, male gender, and immunosuppression represent most of the causes of this [...] Read more.
Non-melanoma skin cancers (NMSC) form the majority of skin cancers, with basal cell carcinoma (BCC) being the most common and cutaneous squamous cell carcinoma (cSCC) being second. Prolonged ultraviolet (UV) exposure, aging, male gender, and immunosuppression represent most of the causes of this category of diseases. BCCs and cSCCs both include different types of skin cancers, such as nodular or morpheaform BCC or flat cSCC. Locally advanced and metastatic NMSCs cannot be treated surgically; thus, systemic therapy (TKI and Immunotherapy) is needed. Interestingly, NMSCs are frequently linked to abnormal Hedgehog (HH) signaling which most systemic immunotherapies for these cancers are based upon. Of note, the first line therapies of BCC, sonidegib and vismodegib, are HH inhibitors. Programmed death receptor 1 antibody (PD-1) inhibitors such as cemiplimab, pembrolizumab, and nivolumab have been approved for the treatment of cSCC. Thus, this paper reviews the epidemiology, risk factors, clinical features, and treatment options for both BCC and cSCC. Full article
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