ArticleProceedings of the National Academy of Sciences of the United States of America2010
Melanocytes are deficient in repair of oxidative DNA damage and UV-induced photoproducts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 119 citations in OpenAlex.
- Metabolic Responses of Melanocytes and Melanoma Cells to UVA Radiation and Phytocannabinoids Exposure.Antioxidants (Basel, Switzerland) · 2026Article
- Genotype-Encoded UV Sensitivity in iPSC-Derived Human Melanocytes Reveals MX2 as a Physiological Amplifier of p53/p38-Mediated DNA Damage Signaling.International journal of molecular sciences · 2026Article
- UVA-induced DNA damage and mutations in human melanocytes: relevance for melanoma mutations.Nucleic acids research · 2025Article
- Natural protection against oxidative stress in human skin melanocytes.Communications biology · 2025Review
- The small molecule ML233 is a direct inhibitor of tyrosinase function.Communications biology · 2025Article
- The small molecule ML233 is a direct inhibitor of tyrosinase function.bioRxiv : the preprint server for biology · 2025Article
- Targeting Dectin-1 and or VISTA enhances anti-tumor immunity in melanoma but not colorectal cancer model.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Review
- The Impact of Antioxidants on Vitiligo and Melasma: A Scoping Review and Meta-Analysis.Antioxidants (Basel, Switzerland) · 2023Article
- UVA Radiation, DNA Damage, and Melanoma.ACS omega · 2022Review
- Comparative Study of Δ9-Tetrahydrocannabinol and Cannabidiol on Melanogenesis in Human Epidermal Melanocytes from Different Pigmentation Phototypes: A Pilot Study.Journal of xenobiotics · 2022Article
- Nucleotide excision repair: a versatile and smart toolkit.Acta biochimica et biophysica Sinica · 2022Review
- XPG: a multitasking genome caretaker.Cellular and molecular life sciences : CMLS · 2022Review
- Article
- Immunomodulatory Effects of BRAF, MEK, and CDK4/6 Inhibitors: Implications for Combining Targeted Therapy and Immune Checkpoint Blockade for the Treatment of Melanoma.Frontiers in immunology · 2021Review
- The involvement of nucleotide excision repair proteins in the removal of oxidative DNA damage.Nucleic acids research · 2020Review
- A Framework of Major Tumor-Promoting Signal Transduction Pathways Implicated in Melanoma-Fibroblast Dialogue.Cancers · 2020Review
- UVA influenced the SIRT1-miR-27a-5p-SMAD2-MMP1/COL1/BCL2 axis in human skin primary fibroblasts.Journal of cellular and molecular medicine · 2020Article
- Solar ultraviolet-induced DNA damage response: Melanocytes story in transformation to environmental melanomagenesis.Environmental and molecular mutagenesis · 2020Review
- Effects and Mechanism of Nicotinamide Against UVA- and/or UVB-mediated DNA Damages in Normal Melanocytes.Photochemistry and photobiology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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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Registered trials
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