학술논문
Twist and p53 reciprocally regulate target genes via direct interaction.
Document Type
Article
Author
Source
Subject
*GENES
*DEOXYRIBOSE
*GENE expression
*TRANSCRIPTION factors
*DNA
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*
*
*
Language
ISSN
0950-9232
Abstract
Twist is basic helix-loop-helix transcription factor that binds to E-boxes in gene promoters. Twist possesses an oncogenic function by interfering with the tumor suppressor function of p53. Using a membrane pull-down assay, we found that Twist directly interacts with p53 and that this interaction underlies the inhibitory effects on p53 target gene expression. Twist interacted with the DNA-binding domain of p53 and suppressed the DNA-binding activity of p53. Transcriptional activation of the p21 promoter by p53 was significantly repressed by the expression of Twist. On the other hand, p53 interacted with the N-terminal domain of Twist and repressed Twist-dependent YB-1 promoter activity. Importantly, we found that p53-dependent growth suppression was canceled by the expression of either Twist or YB-1. Thus, our data suggest that Twist inhibits p53 function via a direct interaction with p53.Oncogene (2008) 27, 5543–5553; doi:10.1038/onc.2008.176; published online 26 May 2008 [ABSTRACT FROM AUTHOR]