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Paracrine regulation of melanocyte genomic stability: a focus on nucleotide excision repair
Author(s) -
Jarrett Stuart Gordon,
Carter Katharine Marie,
D'Orazio John August
Publication year - 2017
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/pcmr.12582
Subject(s) - nucleotide excision repair , dna damage , dna repair , melanocyte , biology , microbiology and biotechnology , mutagenesis , xeroderma pigmentosum , melanocortin 1 receptor , genome instability , melanoma , dna , mutation , cancer research , genetics , gene , phenotype
Summary 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.