NDLI: C/EBP expression is downregulated in human nonmelanoma skin cancers and inactivation of C/EBP confers susceptibility to UVB-induced skin squamous cell carcinomas.

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C/EBP expression is downregulated in human nonmelanoma skin cancers and inactivation of C/EBP confers susceptibility to UVB-induced skin squamous cell carcinomas.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Thompson, Elizabeth A. Zhu, Songyun Hall, Jonathan R. House, John S. Ranjan, Rakesh Burr, Jeanne A. He, Yu-Ying Owens, David M. Smart, Robert C.
Description	Country affiliation: United States Author Affiliation: Thompson EA ( Cell Signaling and Cancer Group, Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, North Carolina 27695-7633, USA.)
Abstract	Human epidermis is routinely subjected to DNA damage induced by UVB solar radiation. Cell culture studies have revealed an unexpected role for C/EBP (CCAAT/enhancer-binding protein- ) in the DNA damage response network, where C/EBP is induced following UVB DNA damage, regulates the G(1) checkpoint, and diminished or ablated expression of C/EBP results in G(1) checkpoint failure. In the current study we observed that C/EBP is induced in normal human epidermal keratinocytes and in the epidermis of human subjects exposed to UVB radiation. The analysis of human skin precancerous and cancerous lesions (47 cases) for C/EBP expression was conducted. Actinic keratoses, a precancerous benign skin growth and precursor to squamous cell carcinoma (SCC), expressed levels of C/EBP similar to normal epidermis. Strikingly, all invasive SCCs no longer expressed detectable levels of C/EBP . To determine the significance of C/EBP in UVB-induced skin cancer, SKH-1 mice lacking epidermal C/EBP (CKO ) were exposed to UVB. CKO mice were highly susceptible to UVB-induced SCCs and exhibited accelerated tumor progression. CKO mice displayed keratinocyte cell cycle checkpoint failure in vivo in response to UVB that was characterized by abnormal entry of keratinocytes into S phase. Our results demonstrate that C/EBP is silenced in human SCC and loss of C/EBP confers susceptibility to UVB-induced skin SCCs involving defective cell cycle arrest in response to UVB.
File Format	HTM / HTML
ISSN	0022202X
e-ISSN	15231747
DOI	10.1038/jid.2011.31
Journal	Journal of Investigative Dermatology
Issue Number	6
Volume Number	131
Language	English
Publisher	Elsevier
Publisher Date	2011-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Dermatology Ccaat-enhancer-binding Protein-alpha Physiology Carcinoma, Squamous Cell Etiology Neoplasms, Radiation-induced Skin Neoplasms Ultraviolet Rays Adverse Effects Animals Chemistry Cell Cycle Cells, Cultured Genes, P53 Keratosis, Actinic Metabolism Mice Mice, Hairless Mice, Inbred C57bl Mutation Precancerous Conditions Skin Radiation Effects Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology Dermatology

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C/EBPα Expression Is Downregulated in Human Nonmelanoma Skin Cancers and Inactivation of C/EBPα Confers Susceptibility to UVB-Induced Skin Squamous Cell Carcinomas

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C/EBP expression is downregulated in human nonmelanoma skin cancers and inactivation of C/EBP confers susceptibility to UVB-induced skin squamous cell carcinomas.

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C/EBP expression is downregulated in human nonmelanoma skin cancers and inactivation of C/EBP confers susceptibility to UVB-induced skin squamous cell carcinomas.