The DOI matches its Crossref record; 38 of the 40 references it cites were found in a registry or an index.
Melanocytes are deficient in repair of oxidative DNA damage and UV-induced photoproducts
Open accessAbstract
Melanomas occur mainly in sunlight-exposed skin. Xeroderma pigmentosum (XP) patients have 1,000-fold higher incidence of melanoma, suggesting that sunlight-induced “bulky” photoproducts are responsible for melanomagenesis. Sunlight induces a high level of reactive oxygen species in melanocytes (MCs); oxidative DNA damage (ODD) may thus also contribute to melanomagenesis, and XP gene products may participate in the repair of ODD. We examined the effects of melanin on UVA (320–400 nm) irradiation-induced ODD and UV photoproducts and the repair capacity in MC and XP cells for ODD and UV-induced photoproducts. Our findings indicate that UVA irradiation induces a significantly higher amount of formamidopyrimidine glycosylase-sensitive ODD in MCs than in normal human skin fibroblasts (NHSFs). In contrast, UVA irradiation induces an insignificant amount of UvrABC-sensitive sites in either of these two types of cells. We also found that, compared to NHSFs, MCs have a reduced repair capacity for ODD and photoproducts; H 2 O 2 modified- and UVC-irradiated DNAs induce a higher mutation frequency in MCs than in NHSFs; and, XP complementation group A (XPA), XP complementation group C, and XP complementation group G cells are deficient in ODD repair and ODD induces a higher mutation frequency in XPA cells than in NHSFs. These results suggest that: ( i ) melanin sensitizes UVA in the induction of ODD but not bulky UV photoproducts; ( ii ) the high susceptibility to UVA-induced ODD and the reduced DNA repair capacity in MCs contribute to carcinogenesis; and ( iii ) the reduced repair capacity for ODD contributes to the high melanoma incidence in XP patients.
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“This was recently illustrated for melanocytes that are more susceptible than other cell types to UVA-induced oxidatively generated damage to DNA both as isolated cells (89,116) and in pigmented mice (117).”
From Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions† (2012) · cites this paper as [116]
In the citing paper
“Melanocytes have diminished repair of UVA-induced oxidative damage, as melanin acts as a photosensitizer to UVA68.”
From Mechanisms and prevention of UV‐induced melanoma (2018) · cites this paper as [68]
Citations
Cites
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Cited by
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Melanoma: from mutations to medicine
Tsao, H., Chin, L., Garraway, L. A., & Fisher, D. E. (2012) · Genes & Development · doi:10.1101/gad.191999.112 · Cited by 496
Sunlight damage to cellular DNA: focus on oxidatively generated lesions
Schuch, A. P., Moreno, N. C., Schuch, N. J., Menck, C. F. M., & Garcia, C. C. M. (2017) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2017.01.029 · Cited by 436
Formation of UV-induced DNA damage contributing to skin cancer development
Cadet, J., & Douki, T. (2018) · Photochemical & Photobiological Sciences · doi:10.1039/c7pp00395a · Cited by 435
Melanocytes as Instigators and Victims of Oxidative Stress
Denat, L., Kadekaro, A. L., Marrot, L., Leachman, S. A., & ABDEL‐MALEK, Z. A. (2014) · Journal of Investigative Dermatology · doi:10.1038/jid.2014.65 · Cited by 429
Mechanisms and prevention of UV‐induced melanoma
Sample, A., & He, Y. (2018) · Photodermatology, Photoimmunology & Photomedicine · doi:10.1111/phpp.12329 · Cited by 372
Metadata
- Authors
- Wang, H.-T., Choi, B., & Tang, M.-S.
- Affiliations
- New York University (US)
- ORCID
- Wang, Hsiang-Tsui
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-06-21
- Volume
- 107
- Issue
- 27
- Pages
- 12180-12185
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2901481
- OpenAlex
- W2113840211
- Cited by
- 119
- References
- 40
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 4 · 2023: 6 · 2022: 5 · 2021: 3 · 2020: 7 · 2019: 4 · 2018: 8 · 2017: 8 · 2016: 8 · 2015: 4 · 2014: 14 · 2013: 13 · 2012: 11
- FWCI
- 5.47
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (CA99007, ES00260.)
- National Cancer Institute (R01CA114541, CA99007, CA114541)
- National Institute of Environmental Health Sciences (ES00260, ES014641, P30ES000260, R01ES014641)
- Brookhaven National Laboratory
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › melanin and skin pigmentation
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Keywords
- melanocytes, oxidative DNA damage, UV photoproducts, xeroderma pigmentosum, melanoma, melanin, UVA irradiation, DNA repair, XPA, XPG, XPC, formamidopyrimidine glycosylase, reactive oxygen species, mutation frequency, melanomagenesis
- MeSH terms
- 8-Hydroxy-2'-Deoxyguanosine, Cells, Cultured, Deoxyguanosine, DNA Damage, DNA Repair, Dose-Response Relationship, Drug, Fibroblasts, Humans, Hydrogen Peroxide, Melanins, Melanocytes, Skin, Ultraviolet Rays, Oxidants, Oxidative Stress, DNA-Formamidopyrimidine Glycosylase
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