Fas Ligand: A Sensor for DNA Damage Critical in Skin Cancer Etiology

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 r...

Full description

Saved in:
Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1999-08, Vol.285 (5429), p.898-900
Main Authors: Hill, Laurie L., Ouhtit, Allal, Loughlin, Susan M., Kripke, Margaret L., Ananthaswamy, Honnavara N., Owen-Schaub, Laurie B.
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Biological and medical sciences
Cancer
Causes of
Cell physiology
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Cells
Codons
Deoxyribonucleic acid
DNA
DNA Damage
Epidermal Cells
Epidermis
Epidermis - metabolism
Epidermis - radiation effects
Etiology
Fas Ligand Protein
fas Receptor - genetics
fas Receptor - physiology
Feedback (Response)
Fundamental and applied biological sciences. Psychology
Genes, p53
Genetic mutation
Keratinocytes
Keratinocytes - cytology
Keratinocytes - metabolism
Keratinocytes - radiation effects
Membrane Glycoproteins - genetics
Membrane Glycoproteins - physiology
Mice
Mice, Inbred C3H
Molecular and cellular biology
Mutation
Physiological aspects
Proofreading
Skin
Skin cancer
Skin cancers
Skin Neoplasms - etiology
Skin Neoplasms - pathology
Sunburn
Sunburn & sun tanning
T lymphocytes
Ultraviolet Rays
Up-Regulation
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.285.5429.898