Effect of oxidative DNA damage in promoter elements on transcription factor binding
Open accessAbstract
Reactive oxygen species produced by endogenous metabolic activity and exposure to a multitude of exogenous agents impact cells in a variety of ways. The DNA base damage 8-oxodeoxyguanosine (8-oxodG) is a prominent indicator of oxidative stress and has been well-characterized as a premutagenic lesion in mammalian cells and putative initiator of the carcinogenic process. Commensurate with the recent interest in epigenetic pathways of cancer causation we investigated how 8-oxodG alters the interaction between cis elements located on gene promoters and sequence-specific DNA binding proteins associated with these promoters. Consensus binding sequences for the transcription factors AP-1, NF-kappaB and Sp1 were modified site-specifically at guanine residues and electrophoretic mobility shift assays were performed to assess DNA-protein interactions. Our results indicate that whereas a single 8-oxodG was sufficient to inhibit transcription factor binding to AP-1 and Sp1 sequences it had no effect on binding to NF-kappaB, regardless of its position. We conclude from these data that minor alterations in base composition at a crucial position within some, but not all, promoter elements have the ability to disrupt transcription factor binding. The lack of inhibition by damaged NF-kappaB sequences suggests that DNA-protein contact sites may not be as determinative for stable p50 binding to this promoter as other, as yet undefined, structural parameters.
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8oxoG can repress gene transcription through multiple mechanisms, including blocking transcription factor binding, recruiting chromatin remodelers that methylate gene promoters, and erroneous BER that can result in single nucleotide variations.
“8oxoG is capable of repressing gene transcription through many mechanisms, including blocking transcription factor binding (Ghosh & Mitchell, 1999; Moore et al, 2016), recruiting chromatin remodelers that result in the methylation of gene promoters(Wang et al, 2018b; Xia et al, 2017, 4), and erroneous repair through BER, which could result in single nucleotide variations (SNVs).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Ghosh & Mitchell, 1999
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- Authors
- Ghosh, R., & Mitchell, D. L.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- Mitchell, D. L.
- Venue
- Nucleic Acids Research
- Publisher
- Oxford University Press (OUP)
- Published
- 1999-08-01
- Volume
- 27
- Issue
- 15
- Pages
- 3213-3218
- ISSN
- 0305-1048 (ISSN-L)
- 1362-4962
- PMC
- PMC148550
- OpenAlex
- W2127761639
- Cited by
- 152
- References
- 48
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 6 · 2022: 6 · 2021: 7 · 2020: 13 · 2019: 6 · 2018: 5 · 2017: 7 · 2016: 6 · 2015: 4 · 2014: 5 · 2013: 2 · 2012: 8
- FWCI
- 1.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nucleic Acids Research (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01es007953-03)
- National Institute of Environmental Health Sciences (ES07953)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- 8-hydroxy-2'-deoxyguanosine, oxidative DNA damage, promoter elements, transcription factor binding, AP-1, NF-κB, Sp1, reactive oxygen species, oxidative stress, epigenetic carcinogenesis, protein-DNA interactions, guanine modification
- MeSH terms
- Base Sequence, Binding Sites, Deoxyguanine Nucleotides, DNA, DNA Damage, DNA-Binding Proteins, Humans, Oxidation-Reduction, Promoter Regions, Genetic, Protein Binding, Transcription Factors, Mutagenesis, Site-Directed, NF-kappa B, Sp1 Transcription Factor, Consensus Sequence, Transcription Factor AP-1, DNA Footprinting, DNA Methylation, Response Elements
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