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Cited by 120DNA Repair Mechanismsmelanin and skin pigmentationSkin Protection and Aging

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

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Wang, Hsiang-Tsui, Choi, Bongkun, Tang, Moon-shong·2010·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.1005244107PMC PMC2901481
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Abstract

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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  1. 10.1001/archderm.1994.01690080084012 · DOI · Paper page
  2. E Friedberg, et al. DNA Repair and Mutagenesis (ASM, Washington, DC), pp. 9–69 (2006).

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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
DOI
10.1073/pnas.1005244107
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
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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