Redox Signaling in Cancer: Mechanisms and Therapeutic Opportunities

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 578

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Guest Editor
Department of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju 37224, Republic of Korea
Interests: ROS; cancer; natural compound; therapeutic; ferroptosis
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Special Issue Information

Dear Colleagues,

Oxidative stress plays a critical role in the development and progression of various cancers. Reactive oxygen species (ROS), when produced in excess, can damage DNA, proteins, and lipids, thereby promoting tumorigenesis. However, recent studies have highlighted the dual role of ROS in cancer, suggesting that elevated oxidative stress can also be exploited for therapeutic purposes by inducing cancer cell death. This Special Issue aims to present the latest research findings on the role of oxidative stress in cancer biology, including but not limited to ROS-mediated signaling pathways, redox regulation, antioxidant defense mechanisms, and oxidative stress-induced cell death (e.g., apoptosis, ferroptosis). We especially welcome original research and reviews that explore the therapeutic potential of natural compounds and targeted interventions that modulate oxidative stress in cancer. Contributions that elucidate the molecular mechanisms underlying oxidative stress-related processes and discuss clinical implications are also encouraged.

We look forward to receiving your valuable contributions to this Special Issue.

Prof. Dr. Myoung Ok Kim
Guest Editor

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Keywords

  • oxidative stress
  • cancer
  • reactive oxygen species (ROS)
  • redox signaling
  • natural compounds
  • ferroptosis

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Published Papers (1 paper)

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Research

18 pages, 4938 KiB  
Article
Isoquercitrin Suppresses Esophageal Squamous Cell Carcinoma (ESCC) by Inducing Excessive Autophagy and Promoting Apoptosis via the AKT/mTOR Signaling Pathway
by Zhibin Liu, Ke Huang, Hai Huang, Eungyung Kim, Hyeonjin Kim, Chae Yeon Kim, Dong Joon Kim, Sang In Lee, Sangsik Kim, Do Yoon Kim, Kangdong Liu, Zae Young Ryoo, Mee-Hyun Lee, Lei Ma and Myoung Ok Kim
Antioxidants 2025, 14(6), 694; https://doi.org/10.3390/antiox14060694 - 8 Jun 2025
Viewed by 484
Abstract
Esophageal squamous cell carcinoma (ESCC), one of the most frequent malignant tumors of the digestive system, is marked by a poor prognosis and high mortality rate. There is a critical need for effective therapeutic strategies with minimal side effects. Isoquercitrin (IQ) is a [...] Read more.
Esophageal squamous cell carcinoma (ESCC), one of the most frequent malignant tumors of the digestive system, is marked by a poor prognosis and high mortality rate. There is a critical need for effective therapeutic strategies with minimal side effects. Isoquercitrin (IQ) is a natural compound with potent antioxidant properties in cancer and cardiovascular diseases. However, its specific effects and mechanisms in ESCC remain largely unexplored. This study aims to investigate the effects of IQ in ESCC cells and elucidate the mechanisms underlying its therapeutic effects. Specifically, its impact on cell proliferation, colony formation, migration, and invasion was assessed using cell viability assay, morphology, transwell, and colony formation assays. The effects on apoptosis were evaluated by flow cytometry, while immunofluorescence (IF) staining and Western blotting were performed to confirm the underlying mechanisms. The in vivo anti-cancer effects of IQ were then evaluated using a xenograft tumor model. Our results demonstrate that IQ inhibits ESCC cell growth and colony formation while promoting its apoptosis by enhancing caspase activation and downregulating Bcl-2 expression. Furthermore, IQ suppresses cell migration by modulating the epithelial–mesenchymal transition-related proteins. Additionally, IQ induces excessive autophagy by promoting reactive oxygen species accumulation and inhibiting the AKT/mTOR signaling pathway. Importantly, IQ effectively reduces tumor growth in vivo, highlighting its potential as a therapeutic agent for ESCC. Full article
(This article belongs to the Special Issue Redox Signaling in Cancer: Mechanisms and Therapeutic Opportunities)
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