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: 28 February 2026 | Viewed by 6400

Special Issue Editors


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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

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
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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

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Keywords

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

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Published Papers (3 papers)

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Research

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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 1 | Viewed by 1738
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
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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 5 | Viewed by 2607
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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