p21/CDKN1A Mediates Negative Regulation of Transcription by p53
Open accessAbstract
The tumor suppressor p53 regulates transcription positively and negatively, depending on the target gene. Whereas p53 induces transcription through direct interaction with promoter DNA, the mechanism of p53-mediated transcriptional repression is less well understood. Early reports described the alleviation of p53-mediated repression by inhibitors of apoptosis, suggesting that negative regulation of transcription might occur only in conjunction with programmed cell death. More recently, it has been proposed that certain genes, such as survivin, are repressed by direct association of p53 with their promoters, followed by recruitment of a repressor complex. We show here that p53-mediated negative regulation of transcription could occur independently of apoptosis. In contrast, the amino-terminal transactivation domain of p53 was required for negative regulation of transcription. Similarly, the p53 homologue p73 diminished the expression of survivin and stathmin, depending on its transactivation domain. Mutation of the putative p53 binding site within the survivin promoter did not impair its repression. These observations raised the hypothesis that activation of an effector gene might be required for repression by p53. Strikingly, when the p53-inducible p21/CDKN1A gene was deleted, p53 no longer repressed any one among 11 genes that it down-regulates otherwise. Most of these genes were also repressed by ectopic p21 in the absence of p53. Overexpressed c-Myc reduced the transcription of p21/CDKN1A and impaired p53-mediated repression but did not abolish repression by ectopic p21. Taken together, these results strongly suggest that increased expression of p21/CDKN1A is necessary and sufficient for the negative regulation of gene expression by p53.
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Numerous cell cycle genes are downregulated via the p53-p21 pathway.
“Following these reports, numerous cell cycle genes were found to be downregulated via the p53-p21 pathway.92, 93, 94, 95, 96, 97”
From Census and evaluation of p53 target genes (2017) · cites this paper as [92]
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Self-citation
- Authors
- Löhr, K., Möritz, C., Contente, A., & Dobbelstein, M.
- Affiliations
- Philipps University of Marburg (DE)
- Corresponding author
- Dobbelstein, Matthias
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2003-08
- Volume
- 278
- Issue
- 35
- Pages
- 32507-32516
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2150945637
- Cited by
- 227
- References
- 75
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 2 · 2021: 9 · 2020: 6 · 2019: 6 · 2018: 11 · 2017: 7 · 2016: 12 · 2015: 9 · 2014: 15 · 2013: 14 · 2012: 11
- FWCI
- 6.46
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, cc-by)
- Funders
- Wilhelm Sander-Stiftung
- Deutsche Forschungsgemeinschaft
- FAZIT Stiftung
- Deutsche Krebshilfe
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p53, CDKN1A/p21, transcriptional repression, p53 transactivation domain, p73, survivin, stathmin, c-Myc, tumor suppressor regulation, gene expression regulation, p53 binding sites
- MeSH terms
- Tumor Protein p73, Survivin, Adenoviridae, Amino Acid Sequence, Base Sequence, Binding Sites, Cell Line, DNA-Binding Proteins, Gene Expression Regulation, Genetic Vectors, Humans, Microtubule Proteins, Microtubule-Associated Proteins, Mitochondria, Molecular Sequence Data, Mutation, Neoplasm Proteins, Nuclear Proteins, Phosphoproteins, Plasmids, Time Factors, Transcription, Genetic, Transfection, Immunoblotting, Transcriptional Activation, Genes, Tumor Suppressor, Genes, p53, Tumor Suppressor Protein p53, Cyclins, Proto-Oncogene Proteins c-myc, Apoptosis, Gene Deletion, Protein Structure, Tertiary, Reverse Transcriptase Polymerase Chain Reaction, Tumor Suppressor Proteins, Cyclin-Dependent Kinase Inhibitor p21, Stathmin, Inhibitor of Apoptosis Proteins
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