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Antioxidants
Special Issues
Oxidative Stress and Inflammation in Cancer Biology
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Oxidative Stress and Inflammation in Cancer Biology

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 (28 February 2026) | Viewed by 16124

Special Issue Editors

Dr. Jorge Sastre-Serra

E-Mail Website
Guest Editor
1. Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d’Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, Palma, Illes Balears, Spain
2. Instituto de Investigación Sanitaria de las Islas Baleares (IdISBa), Hospital Universitario Son Espases, Edificio S, Palma, Illes Balears, Spain
3. CIBER Fisiopatología Obesidad y Nutrición, Instituto Salud Carlos III, Madrid, Spain
Interests: cancer biology; oxidative stress; mitochondria; inflammation; cancer biomarkers; molecular biology; breast cancer; colorectal cancer
Dr. Mercedes Nadal-Serrano

E-Mail Website
Guest Editor
1. Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d’Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, Palma, Illes Balears, Spain
2. Instituto de Investigación Sanitaria de las Islas Baleares (IdISBa), Hospital Universitario Son Espases, Edificio S, Palma, Illes Balears, Spain
Interests: oncology; breast cancer; oxidative stress; mitochondria; senescence; antibody–drug conjugates; drug resistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, leads to cellular and molecular damage that contributes to carcinogenesis. The resulting oxidative damage affects DNA, proteins, and lipids, promoting mutations and oncogenic transformations. Inflammation, often driven and exacerbated by oxidative stress, is a crucial factor in the development and progression of cancer. Chronic inflammation creates a tumor-promoting environment by supporting cellular proliferation, survival, and metastasis.

Key central signaling pathways, including NF-κB, STAT3, and Nrf2, regulate the responses to oxidative stress and inflammation, thereby influencing cancer cell behavior and the tumor microenvironment. Targeting the crosstalk between oxidative stress and inflammation holds promise for novel cancer therapies.

This Special Issue compiles significant research on how oxidative stress and inflammation interconnect in the context of cancer biology. It highlights the potential of antioxidants in modulating these processes and their therapeutic implications. The articles cover a range of topics, from basic molecular mechanisms to translational and clinical research, providing a comprehensive understanding of the role of oxidative stress and inflammation in cancer biology. Through these contributions, this Special Issue aims to provide new insights into the molecular mechanisms of cancer, potentially leading to the development of more effective therapeutic strategies and improved patient outcomes.

Dr. Jorge Sastre-Serra
Dr. Mercedes Nadal-Serrano
Guest Editors

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
  • antioxidant defenses
  • inflammation
  • signaling pathways
  • therapeutic strategies
  • cancer

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Published Papers (6 papers)

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Research

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18 pages, 6615 KB  
Article
Oleocanthal Induces Mitochondrial Dysfunction in Breast Cancer Cell Lines Depending on c-MET Expression
by Sergi Quetglas-Llobera, Pere Miquel Morla-Barcelo, Pilar Roca, Jorge Sastre-Serra and Mercedes Nadal-Serrano
Antioxidants 2026, 15(4), 410; https://doi.org/10.3390/antiox15040410 - 25 Mar 2026
Viewed by 920
Abstract
Oleocanthal (OC), an anti-inflammatory and antioxidant phenolic compound exclusively found in extra virgin olive oil (EVOO), has emerged as a potential anticancer agent through multiple mechanisms of action, yet its impact on key processes such as cellular metabolism remains insufficiently characterized. Here, we [...] Read more.
Oleocanthal (OC), an anti-inflammatory and antioxidant phenolic compound exclusively found in extra virgin olive oil (EVOO), has emerged as a potential anticancer agent through multiple mechanisms of action, yet its impact on key processes such as cellular metabolism remains insufficiently characterized. Here, we investigated the metabolic and mitochondrial responses to OC across different breast cancer molecular subtypes. Triple-negative (MDA-MB-231) and luminal (MCF7, T47D) breast cancer cell lines were treated with OC to evaluate cell viability, cell cycle progression, metabolic enzyme expression, mitochondrial respiration, and mitochondrial network organization. OC responsiveness differed, being highest in MDA-MB-231 and lowest in T47D cells. Lactate dehydrogenase levels decreased in all cell lines, while mitochondrial response varied. MDA-MB-231 mitochondrial function was fully impaired, while MCF7 cells showed increased respiratory activity, with marked mitochondrial fragmentation, and T47D cells largely preserved mitochondrial integrity and function. Notably, the magnitude of OC effects correlated with MET expression, an established target of OC and a prognostic factor associated with reduced relapse-free survival within the triple-negative subtype. Collectively, these findings identify OC as a modulator of cancer cell metabolism and mitochondrial dynamics, with particular relevance in MET-high triple-negative breast cancers. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cancer Biology)
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16 pages, 2689 KB  
Article
Epigenetic Bridge Between Oxidative Balance of Koreans and TCGA Pan-Cancer Risk: Sex-Specific DNA Methylation Signatures
by Sun-Young Kang, Jeong-Soo Gim, Hyunbin Jo and Jeong-An Gim
Antioxidants 2026, 15(3), 386; https://doi.org/10.3390/antiox15030386 - 19 Mar 2026
Viewed by 557
Abstract
Oxidative stress is a hallmark of carcinogenesis, yet the epigenetic mechanisms linking the lifestyle-based Oxidative Balance Score (OBS) to cancer risk remain poorly understood. This study investigated the epigenetic bridge between OBS and pan-cancer susceptibility using a multi-cohort approach integrating population-based and cancer [...] Read more.
Oxidative stress is a hallmark of carcinogenesis, yet the epigenetic mechanisms linking the lifestyle-based Oxidative Balance Score (OBS) to cancer risk remain poorly understood. This study investigated the epigenetic bridge between OBS and pan-cancer susceptibility using a multi-cohort approach integrating population-based and cancer genomic data. We calculated OBS based on 16 dietary and lifestyle factors (including dietary fiber, vitamins, minerals, physical activity, smoking, alcohol, and BMI) for 2749 participants from the Korean Genome and Epidemiology Study (KoGES) and identified OBS-associated CpG sites via epigenome-wide association analysis. These markers were validated against The Cancer Genome Atlas (TCGA) pan-cancer dataset using a novel Hybrid Pi-score (HyPi) to quantify the directional consistency between OBS-driven methylation in healthy individuals and cancer-specific epigenetic alterations across three clinical comparisons: normal vs. tumor, survival outcomes, and tumor stage. We observed profound sex-specific epigenetic signatures, with zero overlap in the top 200 OBS-associated CpG sites between males and females, underscoring fundamental sexual dimorphism in oxidative stress-epigenome interactions. Notably, the top 20 OBS-associated CpGs demonstrated strong directional consistency with multiple cancer types in TCGA, particularly in kidney renal clear cell carcinoma and lung adenocarcinoma, exhibiting methylation patterns inversely correlated with tumorigenesis. Mechanistically, these findings support the role of one-carbon metabolism and vitamin C-dependent DNA demethylation pathways in mediating OBS effects. Our study provides the first evidence of an epigenetic link between lifestyle-based oxidative balance and pan-cancer risk, highlighting the utility of the HyPi score as a novel sex-specific predictive biomarker for cancer prevention. These results suggest that optimizing oxidative balance through precision nutrition may epigenetically modulate cancer susceptibility, opening new avenues for personalized prevention strategies. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cancer Biology)
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14 pages, 1242 KB  
Article
Correlation Between Oxidative Stress and Immune Profiles During Immunotherapy in Metastatic Non-Oncogene-Addicted NSCLC Patients
by Mariangela Peruzzi, Lucrezia Tuosto, Alain Gelibter, Cristina Nocella, Angela Leonardo, Valentina Magri, Chiara Cataldi, Saula Checquolo, Ilaria Grazia Zizzari, Daniele Santini, Roberto Carnevale, Marianna Nuti, Aurelia Rughetti, Giacomo Frati and Chiara Napoletano
Antioxidants 2026, 15(3), 290; https://doi.org/10.3390/antiox15030290 - 26 Feb 2026
Viewed by 674
Abstract
Oxidative stress is considered one of the cancer hallmarks, influencing tumor initiation, progression, and metastasis. High levels of reactive oxygen species (ROS) impair the effectiveness of the immune response in cancer patients. We examined changes in oxidative stress during immunotherapy, exploring the relationship [...] Read more.
Oxidative stress is considered one of the cancer hallmarks, influencing tumor initiation, progression, and metastasis. High levels of reactive oxygen species (ROS) impair the effectiveness of the immune response in cancer patients. We examined changes in oxidative stress during immunotherapy, exploring the relationship between the immune system and clinical parameters related to oxidative burden. Several T-cell and myeloid subsets from 79 metastatic non-oncogene-addicted non-small-cell lung cancer (NSCLC) patients were analyzed using flow cytometry. Additionally, 20 cytokines were measured in serum samples, and sNox2-dp levels, an indicator of NOX2 activity, were assessed by ELISA. Seventy-nine healthy donors served as controls. The data showed that cancer patients had higher levels of sNox2-dp compared to healthy donors (p < 0.0001). Elevated sNox2-dp levels were associated with inflammation-related comorbidities (p = 0.008) and platelet counts (p = 0.03) in NSCLC patients. Furthermore, sNox2-dp displayed a negative correlation with immune cells involved in activation, such as proliferating (Ki67+) CD8+, PD1+ and effector lymphocytes, and a positive correlation with immunosuppressive PMN-MDSCs and inflammatory soluble immune factors, including IL1α, IL1β, IL6, IL10, CCL3, and CCL4. Oxidation levels decreased after immunotherapy (p = 0.04) and increased only in non-responder patients (p = 0.02). Oxidative stress may be indirectly affected by immunotherapy and could serve as a novel tool to identify responding patients in the NSCLC setting. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cancer Biology)
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18 pages, 3287 KB  
Article
The C-X-C Motif Chemokine Ligand 5, Which Exerts an Antioxidant Role by Inducing HO-1 Expression, Is C-X-C Motif Chemokine Receptor 2-Dependent in Human Prostate Stroma and Cancer Cells
by Kang-Shuo Chang, Syue-Ting Chen, Shu-Yuan Hsu, Hsin-Ching Sung, Wei-Yin Lin, Ke-Hung Tsui, Yu-Hsiang Lin, Chen-Pang Hou and Horng-Heng Juang
Antioxidants 2024, 13(12), 1489; https://doi.org/10.3390/antiox13121489 - 5 Dec 2024
Cited by 3 | Viewed by 2273
Abstract
While the C-X-C motif chemokine ligand 5 (CXCL5) is recognized as an inflammatory mediator and a potent attractant for immune cells, its functions within the human prostate remain unclear. This study explored the expression, functions, and regulatory mechanisms of CXCL5 in prostate stroma [...] Read more.
While the C-X-C motif chemokine ligand 5 (CXCL5) is recognized as an inflammatory mediator and a potent attractant for immune cells, its functions within the human prostate remain unclear. This study explored the expression, functions, and regulatory mechanisms of CXCL5 in prostate stroma and cancer cells. CXCL5 secreted from prostate cancer cells enhanced neutrophil migration. CXCL5 induced cell proliferation and invasion of prostate cancer cells in vitro and tumorigenesis in a xenograft animal model. C-X-C motif chemokine receptor 2 (CXCR2) has been identified on the surface of prostate fibroblasts and cancer cells. The supernatant of LNCaP cells or CXCL5 overexpression enhanced the migration and contraction of prostate myofibroblast WPMY-1 cells; however, pretreatment with SB225002, a CXCR2 inhibitor, can reverse these effects. CXCL5 evinces antioxidant properties by upregulating heme oxygenase-1 (HO-1) to counteract H2O2-induced reactive oxygen species (ROS) in a CXCR2-dependent manner in WPMY-1 and prostate cancer cells. Our findings illustrate that CXCL5, through HO-1, plays a role in antioxidation, and determine that the CXCL5/CXCR2/HO-1 pathway facilitates antioxidative communication between fibroblasts and cancer cells in the prostate. Therefore, targeting the CXCL5/CXCR2 signaling pathway could provide a new strategy for managing oxidative stress within the prostate. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cancer Biology)
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Review

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21 pages, 1590 KB  
Review
Oxidative Stress, Parity History, and Remnant Follicles in the Aged Ovary: Insights on Ovarian Cancer Risk and Protection
by Ulises Urzúa, Arnaldo Marín and Enrique A. Castellón
Antioxidants 2025, 14(7), 759; https://doi.org/10.3390/antiox14070759 - 20 Jun 2025
Cited by 3 | Viewed by 3562
Abstract
Ovarian cancer (OC) is the most lethal gynecological cancer globally. Its incidence and mortality consistently rise after menopause. While parity reduces the risk of OC, nulliparity during a woman’s fertile years increases it. Although the association between reproductive history and OC risk is [...] Read more.
Ovarian cancer (OC) is the most lethal gynecological cancer globally. Its incidence and mortality consistently rise after menopause. While parity reduces the risk of OC, nulliparity during a woman’s fertile years increases it. Although the association between reproductive history and OC risk is well-established, the long-term impact of pregnancy on the postmenopausal human ovary has received little to no attention. Parity apparently delays the natural decline of the ovarian reserve, but this association also remains unexplored to date. Based on data from cellular, biochemical, and histological markers, as well as epidemiological studies, transcriptomic analyses, and gene knockout mouse models, we review compelling evidence suggesting a critical intraovarian interplay between the residual ovarian reserve and the ovarian surface epithelium (OSE) in the aged ovary. This interaction appears to be a key factor underlying the protective effect of parity on ovarian cancer (OC) risk. We propose that functional FSHR signaling in the remnant follicles of the aged multiparous ovary somehow counteracts the oxidative stress and subsequent chronic inflammation typically observed in the senescent ovary. This mechanism would minimize DNA damage, thereby lowering the probability of neoplastic transformation in the aged mammalian ovary. The precise mechanism by which pregnancy imprints such a long-term follicle–OSE crosstalk warrants further investigation. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cancer Biology)
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52 pages, 1497 KB  
Review
Oxidative Stress and Inflammation: Drivers of Tumorigenesis and Therapeutic Opportunities
by Meimei Wang, Yaping Xiao, Jie Miao, Xin Zhang, Meng Liu, Longchao Zhu, Hongxin Liu, Xiaoyan Shen, Jihui Wang, Biao Xie and Di Wang
Antioxidants 2025, 14(6), 735; https://doi.org/10.3390/antiox14060735 - 15 Jun 2025
Cited by 46 | Viewed by 6838
Abstract
As two pivotal regulatory factors in cancer biology, oxidative stress and inflammation interact dynamically through complex network mechanisms to influence tumor initiation, progression, and treatment resistance. Oxidative stress induces genomic instability, oncogenic signaling activation, and tumor microenvironment (TME) remodeling via the abnormal accumulation [...] Read more.
As two pivotal regulatory factors in cancer biology, oxidative stress and inflammation interact dynamically through complex network mechanisms to influence tumor initiation, progression, and treatment resistance. Oxidative stress induces genomic instability, oncogenic signaling activation, and tumor microenvironment (TME) remodeling via the abnormal accumulation of reactive oxygen species (ROS) or reactive nitrogen species (RNS). Conversely, inflammation sustains malignant phenotypes by releasing pro-inflammatory cytokines and chemokines and promoting immune cell infiltration. These processes create a vicious cycle via positive feedback loops whereby oxidative stress initiates inflammatory signaling, while the inflammatory milieu further amplifies ROS/RNS production, collectively promoting proliferation, migration, angiogenesis, drug resistance, and immune evasion in tumor cells. Moreover, their crosstalk modulates DNA damage repair, metabolic reprogramming, and drug efflux pump activity, significantly impacting the sensitivity of cancer cells to chemotherapy, radiotherapy, and targeted therapies. This review systematically discusses these advances and the molecular mechanisms underlying the interplay between oxidative stress and inflammation in cancer biology. It also explores their potential as diagnostic biomarkers and prognostic indicators and highlights novel therapeutic strategies targeting the oxidative stress–inflammation axis. The goal is to provide a theoretical framework and translational roadmap for developing synergistic anti-tumor therapies. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cancer Biology)
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