Stepping up melanocytes to the challenge of UV exposure.
Exposure to solar ultraviolet radiation (UV) is the main etiological factor for skin cancer, including melanoma. Cutaneous pigmentation, particularly eumelanin, afforded by melanocytes is the main photoprotective mechanism, as it prevents UV-induced DNA damage in the epidermis. Therefore, maintaining genomic stability of melanocytes is crucial for prevention of melanoma, as well as keratinocyte-derived basal and squamous cell carcinoma. A critical independent factor for preventing melanoma is DNA repair capacity. The response of melanocytes to UV is mediated mainly by a network of paracrine factors that not only activate melanogenesis, but also DNA repair, anti-oxidant, and survival pathways that are pivotal for maintenance of genomic stability and prevention of malignant transformation or apoptosis. However, little is known about the stress response of melanocytes to UV and the regulation of DNA repair pathways in melanocytes. Unraveling these mechanisms might lead to strategies to prevent melanoma, as well as non-melanoma skin cancer.
Department of Dermatology, University of Cincinnati Collage of Medicine, Cincinnati, OH, USA. abdelmza@ucmail.uc.edu
Zalfa A
ZA
Abdel-Malek
Ana Luisa
AL
Kadekaro
Viki B
VB
Swope
D000818:Animals; D004249:DNA Damage; D004260:DNA Repair / Q000502:physiology* / Q000528:radiation effects; D042822:Genomic Instability / Q000528:radiation effects; D006801:Humans; D008544:Melanocytes / Q000378:metabolism*; D008545:Melanoma / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control; D012878:Skin Neoplasms / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control; D014466:Ultraviolet Rays