Protein kinase Cepsilon reveals importance of extrinsic apoptosis in preventing UV carcinogenesis.
UV-induced apoptosis, giving rise to "sunburn cells," has been thought to be primarily cell autonomous (or intrinsic) in nature, triggered by DNA damage and mediated through p53. However, in vivo the microenvironment appears to contribute to UV-induced apoptosis by activating the extrinsic route through death receptors. Protein kinase Cvarepsilon lowers UV-induced expression of Fas and its downstream proteins in this extrinsic route, suppressing apoptosis and enhancing UV carcinogenesis.
de Gruijl
Frank
F
Department of Dermatology, Leiden University Medical Center, Leiden, The Netherlands. f.r.de_gruijl@lumc.nl
D000818:Animals; D017209:Apoptosis / Q000528:radiation effects*; D006801:Humans; D009381:Neoplasms, Radiation-Induced / Q000517:prevention & control*; D051744:Protein Kinase C-epsilon / Q000502:physiology*; D012867:Skin / Q000528:radiation effects*; D012878:Skin Neoplasms / Q000209:etiology / Q000517:prevention & control*; D016159:Tumor Suppressor Protein p53 / Q000502:physiology; D014466:Ultraviolet Rays
D016159:Tumor Suppressor Protein p53; D051744:Protein Kinase C-epsilon