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Antioxidants
Special Issues
Redox Signaling in Cancer: Mechanisms and Therapeutic Opportunities
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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 2143

Special Issue Editor

Prof. Dr. Myoung Ok Kim

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (2 papers)

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Research

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15 pages, 4938 KB  
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
Cited by 1 | Viewed by 1154
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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Review

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27 pages, 827 KB  
Review
The Redox Paradox: Cancer’s Double-Edged Sword for Malignancy and Therapy
by Jyotsna Suresh Ranbhise, Manish Kumar Singh, Songhyun Ju, Sunhee Han, Hyeong Rok Yun, Sung Soo Kim and Insug Kang
Antioxidants 2025, 14(10), 1187; https://doi.org/10.3390/antiox14101187 - 28 Sep 2025
Viewed by 691
Abstract
Reactive oxygen species (ROS) function as critical signaling molecules in cancer biology, promoting proliferation, angiogenesis, and metastasis at controlled levels while inducing lethal damage when exceeding the cell’s buffering capacity. To survive under this state of chronic oxidative stress, cancer cells become dependent [...] Read more.
Reactive oxygen species (ROS) function as critical signaling molecules in cancer biology, promoting proliferation, angiogenesis, and metastasis at controlled levels while inducing lethal damage when exceeding the cell’s buffering capacity. To survive under this state of chronic oxidative stress, cancer cells become dependent on a hyperactive antioxidant shield, primarily orchestrated by the Nrf2, glutathione (GSH), and thioredoxin (Trx) systems. These defenses maintain redox homeostasis and sustain oncogenic signaling, notably through the oxidative inactivation of tumor-suppressor phosphatases, such as PTEN, which drives the PI3K/AKT/mTOR pathway. Targeting this addiction to a rewired redox state has emerged as a compelling therapeutic strategy. Pro-oxidant therapies aim to overwhelm cellular defenses, with agents like high-dose vitamin C and arsenic trioxide (ATO) showing significant tumor-selective toxicity. Inhibiting the master regulator Nrf2 with compounds such as Brusatol or ML385 disrupts the core antioxidant response. Disruption of the GSH system by inhibiting cysteine uptake with sulfasalazine or erastin potently induces ferroptosis, a non-apoptotic cell death driven by lipid peroxidation. Furthermore, the thioredoxin system is targeted by the repurposed drug auranofin, which irreversibly inhibits thioredoxin reductase (TrxR). Extensive preclinical data and ongoing clinical trials support the concept that this reliance on redox adaptation is a cancer-selective vulnerability. Moreover, novel therapeutic strategies, including the expanding field of redox-active metal complexes, such as manganese porphyrins, which strategically leverage the differential redox state of normal versus cancer cells through both pro-oxidant and indirect Nrf2-mediated antioxidative mechanisms (triggered by Keap1 oxidation), with several agents currently in advanced clinical trials, have also been discussed. Essentially, pharmacologically tipping the redox balance beyond the threshold of tolerance offers a rational and powerful approach to eliminate malignant cells, defining a novel frontier for targeted cancer therapy. Full article
(This article belongs to the Special Issue Redox Signaling in Cancer: Mechanisms and Therapeutic Opportunities)
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