E2F7, a novel target, is up-regulated by p53 and mediates DNA damage-dependent transcriptional repression
Open accessAbstract
The p53 tumor suppressor protein is a transcription factor that exerts its effects on the cell cycle via regulation of gene expression. Although the mechanism of p53-dependent transcriptional activation has been well-studied, the molecular basis for p53-mediated repression has been elusive. The E2F family of transcription factors has been implicated in regulation of cell cycle-related genes, with E2F6, E2F7, and E2F8 playing key roles in repression. In response to cellular DNA damage, E2F7, but not E2F6 or E2F8, is up-regulated in a p53-dependent manner, with p53 being sufficient to increase expression of E2F7. Indeed, p53 occupies the promoter of the E2F7 gene after genotoxic stress, consistent with E2F7 being a novel p53 target. Ablation of E2F7 expression abrogates p53-dependent repression of a subset of its targets, including E2F1 and DHFR, in response to DNA damage. Furthermore, E2F7 occupancy of the E2F1 and DHFR promoters is detected, and expression of E2F7 is sufficient to inhibit cell proliferation. Taken together, these results show that p53-dependent transcriptional up-regulation of its target, E2F7, leads to repression of relevant gene expression. In turn, this E2F7-dependent mechanism contributes to p53-dependent cell cycle arrest in response to DNA damage.
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E2F7 is a p53 target gene.
“E2F7 is a p53 target gene117”
From Census and evaluation of p53 target genes (2017) · cites this paper as [117]
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- Authors
- Carvajal, L. A., Hamard, P.-J., Tonnessen, C., & Manfredi, J. J.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2012-07-15
- Volume
- 26
- Issue
- 14
- Pages
- 1533-1545
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC3404382
- OpenAlex
- W2004042953
- Cited by
- 151
- References
- 54
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 13 · 2023: 14 · 2022: 9 · 2021: 10 · 2020: 22 · 2019: 16 · 2018: 9 · 2017: 10 · 2016: 6 · 2015: 9 · 2014: 14 · 2013: 9
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ohio State University
- Johns Hopkins University (HCT116)
- National Cancer Institute (HCT116, F31CA150539, R01CA125741, T32CA078207)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- E2F7, p53, transcriptional repression, DNA damage response, p53 target genes, E2F1, dihydrofolate reductase, cell cycle arrest, tumor suppressor regulation, genotoxic stress
- MeSH terms
- DNA Damage, Humans, Tetrahydrofolate Dehydrogenase, Transcription, Genetic, Up-Regulation, Tumor Suppressor Protein p53, Response Elements, Cell Line, Tumor, E2F7 Transcription Factor, Cell Cycle Checkpoints
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