Abstract
MM-1 has been reported to repress the E-box-dependent transcription activity of c-Myc by recruiting histone deacetylase 1 complex via TIF1beta/KAP1. In this study, to identify target genes for c-Myc-MM-1-TIF1beta, we established rat-1 cells harboring the dominant-negative form of TIF1beta to abrogate the pathway from TIF1beta to MM-1-c-Myc. This cell line, in which transcription activity of c-Myc was activated, was found to be tumorigenic. By DNA-microarray analysis of this cell line, expression and promoter activity of the c-fms oncogene were found to be upregulated. Of the two promoters, pE1 and pE2, in the c-fms gene, pE1 promoter activity was found to be activated in an E-box-dependent manner.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Cells, Cultured
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DNA Primers
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DNA-Binding Proteins / pharmacology*
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Fibroblasts / physiology*
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Genes, Reporter
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Genes, fms / genetics*
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Genes, myc / genetics*
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Luciferases / genetics
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Molecular Sequence Data
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Neoplasms, Experimental / genetics
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Neoplasms, Experimental / pathology
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Promoter Regions, Genetic / genetics
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Proto-Oncogene Proteins c-myc / pharmacology*
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Rats
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Repressor Proteins / pharmacology*
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Reverse Transcriptase Polymerase Chain Reaction
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Transfection
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Tripartite Motif-Containing Protein 28
Substances
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DNA Primers
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DNA-Binding Proteins
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PFDN5 protein, human
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Proto-Oncogene Proteins c-myc
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Repressor Proteins
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Luciferases
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Trim28 protein, rat
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Tripartite Motif-Containing Protein 28