Source:http://linkedlifedata.com/resource/pubmed/id/14517347
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
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| pubmed:dateCreated |
2003-9-30
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| pubmed:abstractText |
UVB radiation is a complete carcinogen able to initiate, promote, and progress keratinocyte cells toward carcinogenesis. Exposure to UVB leads to the propagation of a number of signal transduction pathways resulting in increased DNA binding of transcription factors, including activator protein-1 (AP-1), and subsequent gene expression. To test the hypothesis that AP-1 activation plays a role in the promotion of UVB-induced skin tumors, a dominant negative c-jun (TAM67) mutant transgene was expressed in the epidermis of SKH-1 hairless mice and bred with mice expressing an AP-1 luciferase reporter gene. Single UVB exposure experiments showed a significant decrease in AP-1 activity, as measured by luciferase levels, in mice expressing TAM67 72 h postexposure. Transgenic and nontransgenic littermates were placed into a chronic UVB exposure experiment, three exposures per week for 25 weeks. Expression of TAM67 reduced the number of tumors per mouse by 58% and tumor sizes were 79% smaller than the tumors present in the nontransgenic study group. These tumors were histologically identified as squamous cell carcinomas. TAM67 had no effect on UVB-induced hyperplasia because comparable epidermal thickening was observed in both study groups over a 5-day period post-UVB exposure. Immunohistochemical analysis showed a reduction in the number of cyclin D(1)-expressing cells in squamous cell carcinoma samples removed from the TAM67 study group. These data show that TAM67 can inhibit UVB-induced squamous cell carcinoma formation, suggesting that AP-1 is a good candidate target for the development of new chemoprevention strategies to prevent sunlight-induced skin cancers.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin D1,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun,
http://linkedlifedata.com/resource/pubmed/chemical/TAM67 peptide,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1
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| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
1541-7786
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
1
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
848-54
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| pubmed:dateRevised |
2010-10-1
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| pubmed:meshHeading |
pubmed-meshheading:14517347-Animals,
pubmed-meshheading:14517347-Carcinoma, Squamous Cell,
pubmed-meshheading:14517347-Cyclin D1,
pubmed-meshheading:14517347-Disease Models, Animal,
pubmed-meshheading:14517347-Genes, jun,
pubmed-meshheading:14517347-Hyperplasia,
pubmed-meshheading:14517347-Mice,
pubmed-meshheading:14517347-Mice, Inbred Strains,
pubmed-meshheading:14517347-Mice, Transgenic,
pubmed-meshheading:14517347-Neoplasms, Radiation-Induced,
pubmed-meshheading:14517347-Peptide Fragments,
pubmed-meshheading:14517347-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:14517347-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:14517347-Skin Neoplasms,
pubmed-meshheading:14517347-Time Factors,
pubmed-meshheading:14517347-Transcription Factor AP-1,
pubmed-meshheading:14517347-Transgenes,
pubmed-meshheading:14517347-Ultraviolet Rays
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| pubmed:year |
2003
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| pubmed:articleTitle |
Expression of dominant negative c-jun inhibits ultraviolet B-induced squamous cell carcinoma number and size in an SKH-1 hairless mouse model.
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| pubmed:affiliation |
Department of Radiation Oncology, Arizona Cancer Center, College of Public Health, The University of Arizona, Tucson, AZ, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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