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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: closed (30 November 2025) | Viewed by 6023

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 250 words) can be sent to the Editorial Office for assessment.

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 (5 papers)

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Research

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19 pages, 4673 KB  
Article
Reactive Oxygen Species Drive Cell Migration and PD-L1 Expression via YB-1 Phosphorylation in Pleural Mesothelioma
by Muhammad Hashim, Gerald Timelthaler, Dominik Kirchhofer, Beatrice Irina Kudlacek, Berta Mosleh, Katharina Sinn, Ezzat Mohamed Awad, Mir Alireza Hoda, Bettina Grasl-Kraupp, Balazs Dome, Walter Berger, Georg Krupitza, Karin Schelch and Michael Grusch
Antioxidants 2026, 15(1), 121; https://doi.org/10.3390/antiox15010121 - 17 Jan 2026
Viewed by 363
Abstract
Reactive oxygen species (ROS)-induced aberrant oncogenic signalling has been proposed to mediate the progression and development of pleural mesothelioma (PM). In this study, we demonstrate how ROS promote oncogenic signalling, especially in the context of cell migration and immune evasion via YB-1 phosphorylation [...] Read more.
Reactive oxygen species (ROS)-induced aberrant oncogenic signalling has been proposed to mediate the progression and development of pleural mesothelioma (PM). In this study, we demonstrate how ROS promote oncogenic signalling, especially in the context of cell migration and immune evasion via YB-1 phosphorylation in mesothelial and PM cell models. Xanthine (X)- and xanthine oxidase (XO)-generated ROS exposure led to increased migration and a more elongated cell shape in mesothelial and PM cells in live-cell videomicroscopy analyses. These effects were associated with the enhanced phosphorylation of ERK, AKT, and YB-1 and the elevated gene expression of PD-L1 and PD-L2, which were analysed with immunoblotting and quantitative real-time RT-PCR, respectively. The pharmacological inhibition of AKT (ipatasertib), MEK (trametinib), and RSK (BI-D1870) resulted in the reversal of ROS-induced effects, with the strongest effects observed upon the inhibition of YB-1 phosphorylation by BI-D1870. The results suggest that ROS exposure has a strong impact on cell migration and immune evasion not only in PM cells but also in mesothelial cells, from which PM arises. Interfering with ROS-responsive kinase pathways, particularly YB-1 phosphorylation, could counteract pro-migratory and immune-evasive effects in PM. Full article
(This article belongs to the Special Issue Redox Signaling in Cancer: Mechanisms and Therapeutic Opportunities)
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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 1714
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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50 pages, 3428 KB  
Review
Targeting Oxidative Stress in Carcinogenesis: Oleanolic Acid and Its Molecular Pathways
by Andrzej Günther, Maciej Kulawik, Szymon Sip, Przemysław Zalewski, Donata Jarmołowska-Jurczyszyn, Przemysław Stawicki and Barbara Bednarczyk-Cwynar
Antioxidants 2026, 15(1), 67; https://doi.org/10.3390/antiox15010067 - 4 Jan 2026
Viewed by 649
Abstract
This narrative review aims to systematize the current knowledge on the dual role of reactive oxygen species and reactive nitrogen species in cancer processes, from their physiological function in redox signaling to their pathological impact in oxidative distress. The mechanisms of biomolecule damage, [...] Read more.
This narrative review aims to systematize the current knowledge on the dual role of reactive oxygen species and reactive nitrogen species in cancer processes, from their physiological function in redox signaling to their pathological impact in oxidative distress. The mechanisms of biomolecule damage, particularly DNA, and deregulation of signaling pathways induced by excessive ROS/RNS concentrations, which promote neoplastic transformation, are presented. The importance of diet and endogenous antioxidants in cancer prevention is also discussed, emphasizing the role of natural antioxidants in prevention and adjunctive therapy. In this context, oleanolic acid emerges as a promising compound with dual action modulating oxidative stress, capable of balancing cellular redox responses. We discuss the most important antioxidant mechanisms of oleanolic acid, the interconnection of oxidative stress with carcinogenesis-related pathways, anticancer mechanisms mediated by oxidative stress modulation, and structural modifications and modern application techniques that improve its bioavailability, as well as future perspectives on oleanolic acid research in the context of its antioxidant and anticancer activity. Overall, available experimental and preclinical data indicate that oleanolic acid, through pleiotropic modulation of oxidative stress and signaling networks, holds promise as an adjuvant agent in cancer prevention and therapy. Full article
(This article belongs to the Special Issue Redox Signaling in Cancer: Mechanisms and Therapeutic Opportunities)
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16 pages, 7702 KB  
Review
Redox Modulation in Therapy of Cancer: Some Pros and Cons
by Ljubava D. Zorova, Dmitry S. Semenovich, Savva D. Zorov, Ilya P. Oleynikov, Anastasia S. Kargapoltceva, Dmitry V. Prutskikh, Polina A. Abramicheva, Irina B. Pevzner, Gennady T. Sukhikh and Dmitry B. Zorov
Antioxidants 2025, 14(12), 1496; https://doi.org/10.3390/antiox14121496 - 12 Dec 2025
Viewed by 538
Abstract
Redox potential controls a vast array of biochemical reactions, and its changes influence the transition from normal to pathological states. However, cellular redox potential is primarily assessed after extraction of water-soluble components (reduced and oxidized) from biological material, particularly glutathione, which, due to [...] Read more.
Redox potential controls a vast array of biochemical reactions, and its changes influence the transition from normal to pathological states. However, cellular redox potential is primarily assessed after extraction of water-soluble components (reduced and oxidized) from biological material, particularly glutathione, which, due to its abundance, determines intracellular redox potential. This process involves mechanistic averaging of redox potential values across tissue or cell, although existing data suggest, and sometimes directly indicate, heterogeneity in redox potential both within cells and within tissue. We argue that mitochondria determine cellular redox state, in particular through changes in the state of the mitochondrial reticulum caused by various internal and external factors. We describe the possibilities for regulation of redox status of the cell and organ as a potential therapy for various pathologies, particularly cancer, and propose intensifying efforts to utilize intrinsic redox indicators. We specifically examine the possibility of changes the redox potential in cancer cells through the use of oxidative phosphorylation uncouplers and propose mechanisms by which cancer cells may be killed using uncouplers. Particular attention is paid to the mitochondrial membrane potential as a powerful regulator of cellular metabolism, possibly unrelated to the regulation of reactive oxygen species levels, with the possible existence of a membrane potential sensor in cells. Full article
(This article belongs to the Special Issue Redox Signaling in Cancer: Mechanisms and Therapeutic Opportunities)
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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
Cited by 2 | Viewed by 2188
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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