Transforming growth factor-beta enhances the ultraviolet-mediated stress response in p53-/- keratinocytes
| Autor: | N Neilsen, J I Merryman, D D Stanton |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Chloramphenicol O-Acetyltransferase
Keratinocytes Cancer Research Time Factors Ultraviolet Rays Recombinant Fusion Proteins Gene Expression medicine.disease_cause p38 Mitogen-Activated Protein Kinases Cell Line Transforming Growth Factor beta Cellular stress response medicine Humans Dose-Response Relationship Drug biology Kinase JNK Mitogen-Activated Protein Kinases Dose-Response Relationship Radiation Myelin Basic Protein Transforming growth factor beta Cell cycle Genes p53 Enzyme Activation HaCaT medicine.anatomical_structure Oncology Calcium-Calmodulin-Dependent Protein Kinases Mutation Immunology biology.protein Cancer research Phosphorylation Mitogen-Activated Protein Kinases Carcinogenesis Keratinocyte |
| Zdroj: | International Journal of Oncology. |
| ISSN: | 1791-2423 1019-6439 |
| DOI: | 10.3892/ijo.13.4.781 |
| Popis: | Skin cancer is the most common tumor type in Caucasians, with an incidence that approaches the lifetime risk for all other cancer subtypes combined. The most common predisposing factor in the development of non-melanoma skin cancer is exposure to ultraviolet (UV) radiation in sun-light. UV radiation activates c-Jun amino-terminal kinases (JNK); this kinase pathway is involved in UV-mediated apoptosis and phosphorylation of c-Jun, all of which are part of the cellular stress response. Transforming growth factor-beta1 (TGF-beta1) is an important negative regulator of keratinocyte proliferation and has other pleiotropic effects in these cells. The purpose of these investigations was to decide whether TGF-beta1 activated c-Jun amino-terminal kinases in a spontaneously immortalized human keratinocyte cell line, HaCaT, and if TGF-beta1 modulated the activation of JNK in keratinocytes exposed to ultraviolet C (UVC) radiation. Results from these investigations showed that TGF-beta1 (10 ng/ml) activated JNK within 5 min. Pretreatment with TGF-beta1 enhanced UV-mediated JNK activation and was time- and UV-dose-dependent. Pretreatment with TGF-beta1 also enhanced activity of the c-Jun promoter-reporter construct, TRE(x5)-CAT. These results suggested that TGF-beta1 modulates the response of keratinocytes to ultraviolet radiation and implicates TGF-beta1 as a potential mediator the cellular of stress response in keratinocytes. |
| Databáze: | OpenAIRE |
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