Department of Dermatology, University of Cincinnati Collage of Medicine, Cincinnati, OH, USA.
Pigment Cell Melanoma Res. 2010 Apr;23(2):171-86. doi: 10.1111/j.1755-148X.2010.00679.x. Epub 2010 Feb 1.
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.
暴露于太阳紫外线(UV)辐射是皮肤癌(包括黑色素瘤)的主要病因。黑素细胞产生的皮肤色素沉着,特别是真黑色素,是主要的光保护机制,因为它可以防止表皮中 UV 诱导的 DNA 损伤。因此,维持黑素细胞的基因组稳定性对于预防黑色素瘤以及角质形成细胞衍生的基底细胞癌和鳞状细胞癌至关重要。预防黑色素瘤的一个关键独立因素是 DNA 修复能力。黑素细胞对 UV 的反应主要由旁分泌因子网络介导,该网络不仅激活黑色素生成,还激活 DNA 修复、抗氧化和存活途径,这些途径对于维持基因组稳定性和预防恶性转化或细胞凋亡至关重要。然而,对于黑素细胞对 UV 的应激反应以及黑素细胞中 DNA 修复途径的调节知之甚少。揭示这些机制可能会导致预防黑色素瘤以及非黑色素瘤皮肤癌的策略。