Fas ligand: A sensor for DNA damage critical in skin cancer etiology

被引：205

作者：

Hill, LL ^{[1
]}

Ouhtit, A ^{[1
]}

Loughlin, SM ^{[1
]}

Kripke, ML ^{[1
]}

Ananthaswamy, HN ^{[1
]}

Owen-Schaub, LB ^{[1
]}

机构：

[1] Univ Texas, MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA

来源：

SCIENCE | 1999年 / 285卷 / 5429期

关键词：

D O I：

10.1126/science.285.5429.898

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed "cellular proofreading." Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis, Thus, Fast-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.

引用

页码：898 / 900

页数：3

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