Abstract
Using model spontaneously reverting cell lines, c-jun, junB, junD and c-fos oncogene expression was investigated. c-jun, but not junB, junD or c-fos, was overexpressed in highly tumorigenic clones. The reversion of cells to the non-tumorigenic phenotype resulted in a dramatic decrease in c-jun expression. CAT assays revealed that c-jun overexpression in tumorigenic cells was associated with higher transcription activity. No correlation between c-jun oncogene expression and AP-1 transcription factor activity in tumorigenic and non-tumorigenic clones was found.
MeSH terms
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Animals
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Base Sequence
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Cell Line
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Cell Transformation, Neoplastic*
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Chloramphenicol O-Acetyltransferase / analysis
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Chloramphenicol O-Acetyltransferase / biosynthesis
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Clone Cells
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Gene Expression Regulation*
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Genes, fos
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Genes, jun*
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Metallothionein / genetics
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Mice
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Molecular Sequence Data
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Oligodeoxyribonucleotides
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Promoter Regions, Genetic
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Proto-Oncogene Proteins c-jun / biosynthesis*
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Thymidine Kinase / genetics
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Transfection
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Tumor Cells, Cultured
Substances
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Oligodeoxyribonucleotides
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Proto-Oncogene Proteins c-jun
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Metallothionein
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Chloramphenicol O-Acetyltransferase
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Thymidine Kinase