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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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“Moreover, ROS is recognized as the toxic metabolite of DNA damage.(47) Its production and accumulation affect cell proliferation, differentiation, metabolism, and immune regulation.”
BackgroundDong, X., Yang, F., Xu, X., Zhu, F., Liu, G., Xu, F., Chen, G., Cao, C., Teng, L., Li, X., et al. (2022) · Environmental Toxicology · doi:10.1002/tox.23482 · Cited by 16
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Guo, M., Zhang, W., Niu, S., Shang, M., Chang, X., Wu, T., Zhang, T., Tang, M. X., & Xue, Y. (2022) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2022.110287 · Cited by 16
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“Increased levels of ROS in living cells can damage DNA, RNA, proteins, and healthy cells, resulting in the development and progression of several serious diseases (Srinivas et al. 2019).”
BackgroundJi, X., Jiang, W., Wang, J., Zhou, B., Ding, W., Liu, S., Huang, H., Chen, G., & Sun, X. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1106644 · Cited by 18
“Radiation results in the release of DNA DSBs from tumor cells into the cytoplasm (62).”
BackgroundXu, Y., Bankhead, A., Tian, X., Tang, J., Ljungman, M. E., & Neamati, N. (2020) · Cancer Research · doi:10.1158/0008-5472.can-20-0530 · Cited by 16
“It is well accepted that chemotherapeutics such as cisplatin and mitomycin-C increase ROS levels, which contributes to their genotoxicity (63).”
BackgroundWei, P., Wang, Y., Haiyan, F., Zhang, F., Ji, Z., Zhang, K., Zhang, Q., Jiang, L., Qian, Y., & Fu, Y. (2024) · Small · doi:10.1002/smll.202404463 · Cited by 15
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“85 Microbial metabolites, like secondary bile acids, accumulate in the TME due to microbiota dysbiosis.”
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Mutagenic Consequences of Sublethal Cell Death Signaling
Hawkins, C. J., & Miles, M. A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22116144 · Cited by 15
DRG2 Depletion Promotes Endothelial Cell Senescence and Vascular Endothelial Dysfunction
Le, A.-N., Park, S.-S., Le, M.-X., Lee, U. H., Ko, B. K., Lim, H. R., Yu, R., Choi, S. H., Lee, B. J., Ham, S., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23052877 · Cited by 15
“Oxidative stress causes DNA damage [35] and cellular senescence [13,36].”
BackgroundPeriodic Exposure of Plasma-Activated Medium Alters Fibroblast Cellular Homoeostasis
Bhartiya, P., Kaushik, N., Nguyen, L. N., Bekeschus, S., Masur, K., Weltmann, K., Kaushik, N. K., & Choi, E. H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23063120 · Cited by 17
“The increase in p53 expression may be significant along with the DNA damage response because of redox stress [22,56,57].”
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“Therefore, it was interesting to determine whether the currently investigated compounds stimulate the production of reactive oxygen species (ROS) that may damage DNA integrity and compromise its replication [33].”
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“For example, activating a large number of cell surface receptors increases intracellular hydrogen peroxide levels, thereby mediating downstream effects in a second messenger-like manner (Shi et al., 2017; Moloney and Cotter, 2018; Srinivas et al., 2019).”
BackgroundHe, Y., Chen, H., Li, W., Xu, L. X., Yao, H., Cao, Y., Wang, Z., Zhang, L., Wang, D., & Zhou, D. (2023) · Journal of Nanobiotechnology · doi:10.1186/s12951-023-01970-8 · Cited by 15
“Generally, ionizing radiation induces cell death via two mechanisms - direct interaction with key cellular components to cause DNA damage or production of cytotoxic reactive oxygen species (ROS) [3, 4].”
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Systemic Diseases and Gastrointestinal Cancer Risk
Malkani, N., & Rashid, M. U. (2023) · Journal of Cancer & Allied Specialties · doi:10.37029/jcas.v9i2.473 · Cited by 18
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“Excess ROS can induce DNA damage and affect the DNA damage response.(53) We found that exosomes derived from obese adipose tissue are associated with the increment of ROS production and elevated 8-OHdG and γ-H2AX levels confirm DNA oxidative damage in trophoblast cells.”
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“ROS have been described to stimulate the production of R-loops of both DNA and RNA that appear during cell replication conflicts and are important inducers of genomic instability; 8-OHdG has been linked to the production of these fragments [108].”
BackgroundThe microbiome in the pathogenesis of lung cancer
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“Notably, reactive oxygen species (ROS), a group of highly active and short-lived oxygen-containing molecules produced by the microbiome, mediate DNA damage [72].”
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“Combining GPX4 and NRF2 inhibitors further impairs antioxidant processes, leading to an overload of reactive oxygen species (ROS) and resulting in overwhelming oxidative stress and cell death [31, 32].”
BackgroundDecreasing mitochondrial fission ameliorates HIF-1α-dependent pathological retinal angiogenesis
Huang, S.-Q., Cao, K., Wang, C., Chen, P.-L., Chen, Y., Zhang, Y., Yu, S., Bai, Z.-X., Guo, S., Liao, M., et al. (2024) · Acta Pharmacologica Sinica · doi:10.1038/s41401-024-01262-3 · Cited by 20
“ROS are thought to be cytotoxic and mutagenic, and at high levels, they induce cell death, apoptosis, and senescence [40 – 42].”
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“Free radicals bind to DNA, changing its physical or chemical state and causing DNA breaks, while DNA damage-induced P53 mayarrest the cell cycle and induce apoptosis [57 e 59].”
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Staphylococcus epidermidis biofilm in inflammatory breast cancer and its treatment strategies
Allen-Taylor, D., Boro, G., Cabato, P. M., Mai, C., Nguyen, K., & Rijal, G. (2024) · Biofilm · doi:10.1016/j.bioflm.2024.100220 · Cited by 15
“2) [42,43].”
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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