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ROS and the DNA damage response in cancer
Open accessAbstract
Reactive oxygen species (ROS) are a group of short-lived, highly reactive, oxygen-containing molecules that can induce DNA damage and affect the DNA damage response (DDR). There is unequivocal pre-clinical and clinical evidence that ROS influence the genotoxic stress caused by chemotherapeutics agents and ionizing radiation. Recent studies have provided mechanistic insight into how ROS can also influence the cellular response to DNA damage caused by genotoxic therapy, especially in the context of Double Strand Breaks (DSBs). This has led to the clinical evaluation of agents modulating ROS in combination with genotoxic therapy for cancer, with mixed success so far. These studies point to context dependent outcomes with ROS modulator combinations with Chemotherapy and radiotherapy, indicating a need for additional pre-clinical research in the field. In this review, we discuss the current knowledge on the effect of ROS in the DNA damage response, and its clinical relevance.
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“The most frequently occurring mutations in the tumor suppressor gene TP53 in lung cancer are Guanine → Thymine and Guanine → Adenine transversions (Srinivas et al. 2019; Gibbons et al. 2014).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Srinivas et al. 2019
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Application of Ultrasound Combined with Microbubbles for Cancer Therapy
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“IR can cause a direct effect on DNA or an indirect one, in which DNA damage is mediated by the generation of reactive oxygen species (ROS) [42,43].”
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“A large number of studies have shown that ROS can cause oxidative damage and DNA damage [38], including DNA doublestrand breaks (DSBs) [12], which can alter the sensitivity of tumor cells to chemotherapeutic drugs [39].”
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Metabolic Health, Mitochondrial Fitness, Physical Activity, and Cancer
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“In cancer, high levels of ROS can occur due to excessive metabolic activity and reduced antioxidant capacity [6].”
Experimental Methods for the Biological Evaluation of Nanoparticle-Based Drug Delivery Risks
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“Apoptosis and DNA damage are thought to be caused by excessive free radical production [62].”
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Role of Oxidative Stress in the Occurrence, Development, and Treatment of Breast Cancer
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In Vitro and In Vivo Models for Evaluating the Oral Toxicity of Nanomedicines
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“Cells routinely produce antioxidants, such as reduced glutathione (GSH) and α-lipoic acid, to neutralize excessive ROS and maintain normal functions [68,69].”
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Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence
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Role of eIF5A in Mitochondrial Function
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Applications and enhancement strategies of ROS-based non-invasive therapies in cancer treatment
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“This stress can damage essential cellular components, including DNA, proteins, and lipids, thereby exerting cytotoxic effects [43,44].”
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Cross‐Talk between Oxidative Stress and m6A RNA Methylation in Cancer
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Oxidative stress affects the beginning of the growth of cancer cells through a variety of routes
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“Importantly, excessive ROS generation is known to induce DNA double-strand breaks [26].”
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“Elevated intercellular ROS levels can activate tumor-promoting signals, promote cell proliferation, enhance cell survival, and induce DNA damage [6].”
BackgroundThe Emerging Roles of Rad51 in Cancer and Its Potential as a Therapeutic Target
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Research Progress on the Anti-Aging Potential of the Active Components of Ginseng
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“ROS oxidize nucleoside bases, attack the double bonds of DNA molecules, and induce single- or double-stranded DNA breaks [60,61].”
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Osteoclasts and osteoarthritis: Novel intervention targets and therapeutic potentials during aging
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“Meanwhile, shortened telomeres, DNA damage response signaling pathways, as well as SASP have also been proven to be directly related to ROS (Passos et al., 2010; Srinivas et al., 2019; von Zglinicki, 2002).”
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“Interestingly, ROS trigger microsatellite instability through the induction of DNA damage [31,32].”
BackgroundInterplay between Mitochondrial Metabolism and Cellular Redox State Dictates Cancer Cell Survival
Foo, B. J.-A., Eu, J. Q., Hirpara, J. L., & Pervaiz, S. (2021) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2021/1341604 · Cited by 56
“As such, the dual role of p53 in regulating cellular redox state switches the pendulum from survival to death execution [95].”
Background
Metadata
- Authors
- Srinivas, U. S., Tan, B. W. Q., Vellayappan, B. A., & Jeyasekharan, A. D.
- Affiliations
- National University of Singapore (SG)
- National University Hospital (SG)
- Corresponding author
- Jeyasekharan, Anand D.
- Venue
- Redox Biology
- Publisher
- Elsevier BV
- Published
- 2019-07
- Volume
- 25
- Pages
- 101084
- ISSN
- 2213-2317 (ISSN-L)
- PMC
- PMC6859528
- OpenAlex
- W2906120852
- Cited by
- 2,144
- References
- 153
- Citations by year
- 2026: 217 · 2025: 396 · 2024: 392 · 2023: 381 · 2022: 335 · 2021: 262 · 2020: 132 · 2019: 26
- FWCI
- 10.28
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Redox Biology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- National University of Singapore (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Medical Research Council (NMRC/TA/0052/2016)
- AstraZeneca
- Ministry of Health -Singapore
- Meso Scale Diagnostics
- National Research Foundation Singapore
- Ministry of Education - Singapore
- Janssen Pharmaceuticals
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- reactive oxygen species, DNA damage response, cancer, DNA double-strand breaks, genotoxic stress, anticancer agents, ionizing radiation, radiosensitizers, combination therapy, oxidative DNA damage
- MeSH terms
- Animals, DNA Damage, DNA Repair, Humans, Neoplasms, Tumor Suppressor Protein p53, Apoptosis, Reactive Oxygen Species
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