Paracrine regulation of melanocyte genomic stability: a focus on nucleotide excision repair

Stuart Gordon Jarrett, Katharine Marie Carter, John August D'Orazio

Research output: Contribution to journalReview articlepeer-review

8 Scopus citations

Abstract

UV radiation is a major environmental risk factor for the development of melanoma by causing DNA damage and mutations. Resistance to UV damage is largely determined by the capacity of melanocytes to respond to UV injury by repairing mutagenic photolesions. The nucleotide excision repair (NER) pathway is the major mechanism by which cells correct UV photodamage. This multistep process involves the basic steps of damage recognition, isolation, localized strand unwinding, assembly of a repair complex, excision of the damage-containing strand 3′ and 5′ to the photolesion, synthesis of a sequence-appropriate replacement strand, and finally ligation to restore continuity of genomic DNA. In melanocytes, the efficiency of NER is regulated by several hormonal pathways including the melanocortin and endothelin signaling pathways. Elucidating molecular mechanisms by which melanocyte DNA repair is regulated offers the possibility of developing novel melanoma-preventive strategies to reduce UV mutagenesis, especially in UV-sensitive melanoma-prone individuals.

Original languageEnglish
Pages (from-to)284-293
Number of pages10
JournalPigment Cell and Melanoma Research
Volume30
Issue number3
DOIs
StatePublished - May 2017

Bibliographical note

Publisher Copyright:
© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

Keywords

  • UV photodamage
  • endothelin receptor signaling
  • melanocortin signaling
  • mutagenesis
  • nucleotide excision repair

ASJC Scopus subject areas

  • Oncology
  • General Biochemistry, Genetics and Molecular Biology
  • Dermatology

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