Induction of murine H-rev107 gene expression by growth arrest and histone acetylation: involvement of an Sp1/Sp3-binding GC-box.

H-rev107 is downregulated in many carcinomas and tumor cell lines. Using postconfluent NIH3T3 cells, we demonstrated that growth arrest caused by contact inhibition, but not serum deprivation, increased H-rev107 expression. Furthermore, histone deacetylase inhibitors induced H-rev107 expression in NIH3T3 cells and allowed its reexpression in H-rev107-deficient WEHI 7.1 lymphoma cells. ...
In contrast, no effect of the postconfluent stage or histone deacetylase inhibitors on H-rev107 levels was observed in tumorigenic H-rev107-expressing cell lines, HepG2, HeLa, and SKBR3. Transfections showed that TSA treatment increased luciferase activity 20-fold in NIH3T3 cells. We found that the GC-box at -83/-75 is a key element for H-rev107 induction by TSA and growth arrest, although there were no changes in the pattern and intensity of Sp1/Sp3-binding after induction. These data suggest that contact inhibition of growth and growth arrest caused by histone deacetylase inhibitors probably use the same mechanism to stimulate H-rev107 expression via histone acetylation in NIH3T3 cells and this might contribute to the development of drugs that can induce H-rev107 expression in certain tumors.
Mesh Terms:
3T3 Cells, Acetylation, Animals, Cell Count, Contact Inhibition, DNA-Binding Proteins, Down-Regulation, Gene Expression Regulation, Hela Cells, Histone Deacetylase Inhibitors, Histones, Humans, Intracellular Signaling Peptides and Proteins, Mice, Peroxidases, Peroxiredoxins, Promoter Regions, Genetic, Protein Biosynthesis, Proteins, RNA, Messenger, Reverse Transcriptase Polymerase Chain Reaction, Sp1 Transcription Factor, Sp3 Transcription Factor, Transcription Factors, Transcriptional Activation, Tumor Cells, Cultured, Tumor Suppressor Proteins
Biochem. Biophys. Res. Commun.
Date: May. 31, 2002
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