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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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“Several cytokines, including TGF ‐ β 1, have been shown to promote apoptosis resistance of myofibroblasts (Srinivas et al., 2019).”
Progress in the study of anti-tumor effects and mechanisms of vitexin
Yang, Q., Huan, R., Meng, D., Qi, J., & Xia, L. (2024) · Pharmacological Reports · doi:10.1007/s43440-024-00664-8 · Cited by 11
“ROS are a group of short-lived, highly reactive oxygen-containing molecules that can induce DNA damage and affect DNA damage response [ 63 ].”
Targeting CA9 restricts pancreatic cancer progression through pH regulation and ROS production
Yang, H. J., Tong, X., Wang, W. J., Yu, X., Xu, J., & Shi, S. (2024) · Cellular Oncology · doi:10.1007/s13402-024-01022-9 · Cited by 11
Tu, C., Wang, S., Dai, M.-X., Lai, S.-Q., Huang, Z.-W., Yu, Y.-P., Chen, Y.-B., Zeng, J., Wang, L., & Zhong, Z. (2025) · Molecular Medicine · doi:10.1186/s10020-025-01076-x · Cited by 13
The role of Sestrins in the regulation of the aging process
Fan, X., Zeng, Y. Y., Song, W., Li, J., Ai, S., Yang, D., Mao, X., & Yang, M. (2020) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2020.111251 · Cited by 12
Effects of Iron Chelation in Osteosarcoma
Argenziano, M., Paola, A. D., Tortora, C., Pinto, D., Pota, E., Martino, M. D., Perrotta, S., Rossi, F., & Punzo, F. (2020) · Current Cancer Drug Targets · doi:10.2174/1568009620666201230090531 · Cited by 11
The characterization and biological activities of synthetic N, O-selenized chitosan derivatives
Chen, W., Cheng, H., Jiang, Q., & Xia, W. (2021) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2021.01.084 · Cited by 12
EF24 exerts cytotoxicity against NSCLC via inducing ROS accumulation
Chang, M., Shang, M., Yuan, F., Guo, W., & Wang, C. (2021) · Cancer Cell International · doi:10.1186/s12935-021-02240-z · Cited by 11
Anti-Tumor and Anti-Metastasis Effects of Berbamine-Loaded Lipid Nanoparticles on Pancreatic Cancer
Tang, Z., Yi-Chun, N., Xu, Z., Shi, Y., Liu, Y., Fu, W., Zheng, M., He, H., & Wu, T. (2022) · Anti-Cancer Agents in Medicinal Chemistry · doi:10.2174/1871520622666220501161636 · Cited by 11
Fernandes, C., Palma, E., Silva, F., Belchior, A., Pinto, C. I. G., Guerreiro, J. F., Botelho, H. M., Mendes, F., Raposinho, P., & Paulo, A. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23137238 · Cited by 16
Park, C., Cha, H., Lee, H., Jeong, J.-W., Han, M. H., Song, K. S., Kim, G., Chang, Y., Leem, S., Hyun, J. W., et al. (2022) · General Physiology and Biophysics · doi:10.4149/gpb_2022013 · Cited by 11
Zhu, J., Li, L., Duan, Y., Wu, Y., & Wang, X. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.924210 · Cited by 11
“Frontiers in Oncology 09 lead to a rise in oxidative stress and a drop in antioxidants while the destruction of tumour cells (35, 36).”
BackgroundLiu, L., Cui, J., Chen, S., Zhang, X., Wang, S., & Huang, L. (2022) · The Science of The Total Environment · doi:10.1016/j.scitotenv.2022.160819 · Cited by 12
Oncometabolic role of mitochondrial sirtuins in glioma patients
Haq, M. F. U., Hussain, M. Z., Mahjabeen, I., Akram, Z., Saeed, N., Shafique, R., Abbasi, S. F., & Kayani, M. A. (2023) · PLoS ONE · doi:10.1371/journal.pone.0281840 · Cited by 11
“ROS accumulation also results in mitochondrial DNA lesions, strand breaks and degradation of mitochondrial DNA [95].”
BackgroundMajidi, H. J., Zabihi, E., Arab‐Bafrani, Z., Mir, S. M., & Reiter, R. J. (2023) · 2D Materials · doi:10.1088/2053-1583/acc413 · Cited by 11
“X-ray radiotherapy is considered as one of the main approaches to eradicate breast cancer cells (BCCs) and tumor removal [4, 5].”
Zheng, Z., Wang, X., & Chen, D. (2023) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2023.11924 · Cited by 11
Madrid, A., Martín-Pardillos, A., Bonet‐Aleta, J., Sancho‐Albero, M., Martinez, G., Calzada-Funes, J., Martín‐Duque, P., Santamarı́a, J., & Hueso, J. L. (2023) · Catalysis Today · doi:10.1016/j.cattod.2023.114154 · Cited by 11
“Since the generation of ROS is directly related to the induction of DNA damage, DNA damage response activation and reduction of cell viability was also evaluated [73,74].”
Lee, Y.-P., Lin, C.-R., Chen, S.-S., Chen, R.-J., Wu, Y.-H., Chen, Y., & Huang, B. (2023) · PubMed Central · Cited by 11
Zhou, J., Zhao, R., Zhou, H., Yang, S., Tao, F., Xie, Y., Wang, H., & Yun, J. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1196158 · Cited by 11
“The accumulation of excessive ROS disrupts the integrity of the mitochondrial membrane, causes the opening of mitochondrial membrane transport pores, reduces ΔΨm, and thus leading to mitochondrial pathway-mediated apoptosis (Zorov et al., 2014; Srinivas et al., 2019).”
BackgroundLavado, G., & Cava, R. (2023) · LWT · doi:10.1016/j.lwt.2023.115025 · Cited by 11
Ngamphaiboon, N., Chairoungdua, A., Dajsakdipon, T., & Jiarpinitnun, C. (2023) · Oral Oncology · doi:10.1016/j.oraloncology.2023.106520 · Cited by 13
Peng, H., Zhu, M., Kong, W., Tang, C., Du, J., Huang, Y., & Jin, H. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1161542 · Cited by 11
“mouse model of spontaneous atherosclerosis (Srinivas et al., 2019).”
Gaur, T., Ali, A., Sharma, D., Gupta, S. K., Gota, V., Bagal, B. P., Platzbeckar, U., Mishra, R., Dutt, A., Khattry, N., et al. (2023) · Cellular Signalling · doi:10.1016/j.cellsig.2023.111004 · Cited by 11
Ferguson, D. T., Taka, E., Messeha, S. S., Flores‐Rozas, H., Reed, S. L., Redmond, B. V., Soliman, K. F. A., Kanga, K. J. W., & Darling‐Reed, S. (2024) · Nutrients · doi:10.3390/nu16020300 · Cited by 12
“Further research is needed to fully elucidate the mechanism of DATS and the findings obtained from our results.”
ResultChoukroun, É., Parnot, M., Surmenian, J., Gruber, R., Cohen, N., Davido, N., Simonpieri, A., Savoldelli, C., Afota, F., Mjabber, H. E., et al. (2024) · Bioengineering · doi:10.3390/bioengineering11020191 · Cited by 13
Silva‐Hirschberg, C., Hartman, H., Stack, S., Swenson, S. D., Minea, R. O., Davitz, M. A., Chen, T. C., & Schönthal, A. H. (2019) · Therapeutic Advances in Medical Oncology · doi:10.1177/1758835919891567 · Cited by 11
Huang, M.-F., Pang, L. K., Chen, Y., Zhao, R., & Lee, D. (2021) · Cells · doi:10.3390/cells10112823 · Cited by 12
Epigenetically programmed resistance to chemo- and immuno-therapies
Walker, R. R., Rentia, Z., & Chiappinelli, K. B. (2023) · Advances in cancer research · doi:10.1016/bs.acr.2022.12.001 · Cited by 13
Chen, S., Wang, C., Meng, Y., Li, P., Pan, Y., He, M., & Ni, X. (2024) · International Journal of Nanomedicine · doi:10.2147/ijn.s441418 · Cited by 7
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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