Journal
CELL DEATH AND DIFFERENTIATION
Volume 19, Issue 12, Pages 1992-2002Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2012.89
Keywords
p53; ChIP-seq; repression; Sp1; STAT3; microarray
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Funding
- Swedish Cancer Society
- Swedish Research Council
- Cancer Society of Stockholm
- Karolinska Institutet (ACT! Temacentrum)
- Ragnar Soderberg's Foundation
- Robert Lundberg's memorial foundation
- European Commission
- Russian federal program 'Living systems' [11.519.11.2031]
- BMBF
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The tumor-suppressor p53 can induce various biological responses. Yet, it is not clear whether it is p53 in vivo promoter selectivity that triggers different transcription programs leading to different outcomes. Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed 'p53 default program', that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes. Parallel analysis of gene expression allowed identification of 280 novel p53 target genes, including p53-repressed AURKA. We identified Sp1 as one of the p53 modulators, which confer specificity to p53-mediated transcriptional response upon RITA. Further, we found that STAT3 antagonizes p53-mediated repression of a subset of genes, including AURKA. Cell Death and Differentiation (2012) 19, 1992-2002; doi:10.1038/cdd.2012.89; published online 13 July 2012
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