The shady side of sunlight: current understanding of the mechanisms underlying UV-induction of skin cancers.
The incidence of skin cancer has been rising at an astonishing rate, particularly that of the deadliest skin cancer, melanoma. While the molecular mechanisms of sunlight ultraviolet radiation (UV)-induced non-melanoma skin cancer (NMSC) have been well documented, there is a major gap in our current knowledge of how UV initiates melanoma. However, the components of the retinoblastoma (Rb) pathway, the p53 and the p16 pathways are considered the major targets of UV-induced NMSC and melanoma, respectively. Our recent study has revealed that these two pathways coordinate the early responses to UV radiation in the skin. Here, we review the value of studies targeting these early events of skin carcinogenesis, with specific focus on the critical role of the components of the Rb pathway.
Trappey
Alison
A
Department of Pthology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Fernando
Augusta
A
Gaur
Rajiv
R
Raj
Madhwa
M
Ouhtit
Allal
A
D017209:Apoptosis / Q000187:drug effects*; D019941:Cyclin-Dependent Kinase Inhibitor p16; D004249:DNA Damage / Q000528:radiation effects*; D006801:Humans; D008545:Melanoma / Q000209:etiology*; D009363:Neoplasm Proteins / Q000378:metabolism; D009381:Neoplasms, Radiation-Induced / Q000209:etiology*; D012878:Skin Neoplasms / Q000209:etiology*; D013472:Sunlight / Q000009:adverse effects*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014466:Ultraviolet Rays / Q000009:adverse effects*
C000614131:CDKN2A protein, human; D019941:Cyclin-Dependent Kinase Inhibitor p16; D009363:Neoplasm Proteins; D016159:Tumor Suppressor Protein p53