Van Laethem An, Claerhout Sofie, Garmyn Maria, Agostinis Patrizia
Division of Biochemistry, Catholic University of Leuven, Herestraat 49, B-3000, Belgium.
Int J Biochem Cell Biol. 2005 Aug;37(8):1547-53. doi: 10.1016/j.biocel.2005.02.015. Epub 2005 Mar 8.
Sunburn cells are keratinocytes undergoing apoptosis after they have received a physiological UVB dose that irreversibly and severely damaged their DNA or other chromophores. If these cells would escape programmed cell death, a cancer prone phenotype could arise. On the other hand, if the decision to die is made too prematurely, the proliferative compartment of basal keratinocytes would be inevitably lost, thereby hampering normal skin homeostasis. Pro- and anti-apoptotic mediators carefully control crucial points of the cell death program by regulating complex signalling cascades originating at the cell membrane, the nucleus and the cytoplasm. The balance between survival and apoptogenic factors determines the final cell fate, and growing evidence suggests that the deregulation of this balance by chronic UVB stress, results in the development of skin malignancy. The present paper reviews recent data on the major pathways regulating UVB-induced sunburn cell formation and implicates the deregulation of these pathways in the development of skin cancer.
晒伤细胞是角质形成细胞,在接受了生理剂量的中波紫外线(UVB)后发生凋亡,该剂量会对其DNA或其他发色团造成不可逆的严重损伤。如果这些细胞逃避程序性细胞死亡,可能会出现易患癌症的表型。另一方面,如果过早做出死亡决定,基底角质形成细胞的增殖区室将不可避免地丧失,从而阻碍正常的皮肤稳态。促凋亡和抗凋亡介质通过调节源自细胞膜、细胞核和细胞质的复杂信号级联反应,仔细控制细胞死亡程序的关键点。存活因子和促凋亡因子之间的平衡决定了最终的细胞命运,越来越多的证据表明,长期UVB应激导致这种平衡失调,会引发皮肤恶性肿瘤。本文综述了有关调节UVB诱导的晒伤细胞形成的主要途径的最新数据,并指出这些途径的失调与皮肤癌的发生有关。