Abstract
The exposure of mammalian cells to ultraviolet (UV) irradiation leads to the activation of transcription factors, such as AP-1 and NFkB. We demonstrate that aspirin, a promising cancer chemopreventative agent, inhibited UVC-induced AP-1 activity in JB6 cells. In JB6 cells, UVC stimulated Erks, JNKs and P38 kinase activities; aspirin only inhibited activation of JNKs, but not the other MAP kinases. Since the transcription factor AP-1 is important for the process of tumor promotion, the inhibitory effect of aspirin on AP-1 activation suggests that it can be used as a chemopreventative agent against skin cancer.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Anticarcinogenic Agents / pharmacology
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Aspirin / pharmacology*
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Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
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Cell Line
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Dose-Response Relationship, Drug
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Genes, Reporter
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JNK Mitogen-Activated Protein Kinases
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Mice
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Mitogen-Activated Protein Kinases*
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Recombinant Fusion Proteins / biosynthesis
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Recombinant Fusion Proteins / metabolism
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Transcription Factor AP-1 / drug effects
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Transcription Factor AP-1 / metabolism*
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Transcription Factor AP-1 / radiation effects
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Transfection
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Ultraviolet Rays*
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p38 Mitogen-Activated Protein Kinases
Substances
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Anticarcinogenic Agents
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Recombinant Fusion Proteins
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Transcription Factor AP-1
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Calcium-Calmodulin-Dependent Protein Kinases
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases
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p38 Mitogen-Activated Protein Kinases
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Aspirin