Exp Mol Med.  2005 Oct;37(5):488-491.

Transcription repression of a CCAAT-binding transcription factor CBF/HSP70 by p53

Affiliations
  • 1National Research Laboratory for Cell Cycle Regulation, Department of Microbiology, Dankook University College of Medicine, Cheonan 330-714, Korea. dreamer@dku.edu

Abstract

NF-Y transcription factor binds to CCAAT boxes on promoters of cell cycle regulatory genes such as cdc2, cyclin B, cdc25C, and cyclin A. We previously reported that the DNA binding activity of NF-Y is regulated by p53-p21-cdk2 pathway. CBF/HSP70 was originally identified as a transcription factor binding to the CCAAT box on the hsp70 promoter and mediates transcription repression of hsp70 pro- moter by p53. Recently it was demonstrated that CBF/HSP70 interacts and cooperates with NF-Y. In this study, we found that p53 represses the transcription of CBF/HSP70. Since transactivation ability of NF-Y is regulated in a cell cycle-dependent manner, we examined the transcription of CBF/HSP70 during the cell cycle. After synchronization of a human bladder carcinoma cell lacking functional p53 at early S phase, we infect the cells with adenovirus encoding p53. Cells infected with control virus progressed to S and G2 after release from the arrest. In contrast, cells expressing p53 enter S and G2 phases, but arrest at G2/M. The expression of CBF/HSP70 was induced at S/G2 phase in cells infected with a control virus, but kept to be repressed in cells expressing p53. Thus, these results suggest that p53 suppresses the expression of cell cycle regulatory genes though inhibiting both CCAAT binding factors, CBF/HSP70 and NF-Y.

Keyword

cell cycle; cell cycle proteins; protein p53; transcription factors

MeSH Terms

CCAAT-Binding Factor/*metabolism
Cell Cycle
Cell Line, Tumor
*Down-Regulation
HSP70 Heat-Shock Proteins/*metabolism
Humans
Protein Binding
Research Support, Non-U.S. Gov't
*Transcription, Genetic
Tumor Suppressor Protein p53/genetics/*metabolism
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