Cited by 120Cancer-related Molecular PathwaysTelomeres, Telomerase, and SenescenceGenomics and Chromatin Dynamics

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E2F transcriptional repressor complexes are critical downstream targets of p19ARF/p53-induced proliferative arrest

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Rowland, Benjamin D, Denissov, Serguei G, Douma, Sirith, Stunnenberg, Hendrik G, Bernards, René, Peeper, Daniel S·2002·Cancer Cell

DOI 10.1016/s1535-6108(02)00085-5

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Abstract

The p16(INK4a)/pRB/E2F and p19(ARF)/p53 tumor suppressor pathways are disrupted in most human cancers. Both p19(ARF) and p53 are required for the induction of senescence in primary mouse embryonic fibroblasts (MEFs), but little is known about their downstream targets. Disruption of E2F-mediated transcriptional repression in MEFs caused a general increase in the expression of E2F target genes, including p19ARF. We detected no contribution of E2F-mediated transactivation in this setting, indicating that a predominant role of endogenous E2F in asynchronously growing primary MEFs is to repress its target genes. Moreover, relief of transcriptional repression by E2F rendered MEFs resistant to senescence induced by either p19(ARF), p53, or RAS(V12). Thus, E2F transcriptional repressor complexes are critical downstream targets of antiproliferative p19(ARF)/p53 signaling.

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Authors: Rowland, B. D., Denissov, S. G., Douma, S., Stunnenberg, H. G., Bernards, R., & Peeper, D. S.
Affiliations: The Netherlands Cancer Institute (NL)
Radboud University Nijmegen (NL)
Corresponding author: Bernards, René
ORCID: Rowland, Benjamin D
Stunnenberg, Hendrik G
Bernards, René
Peeper, Daniel S
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2002-07
Volume: 2
Issue: 1
Pages: 55-65
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/s1535-6108(02)00085-5
OpenAlex: W2149068611
Cited by: 120
References: 81
Citations by year: 2026: 1 · 2025: 1 · 2023: 1 · 2022: 2 · 2021: 5 · 2020: 1 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 3 · 2013: 4 · 2012: 1
FWCI: 6.48
Type: journal article
Language: en
Open access: bronze
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Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 4034 d)
Locations: Cancer Cell (publishedVersion)
PubMed (publishedVersion)
Utrecht University Repository (Utrecht University) (submittedVersion, other-oa)
Radboud Repository (Radboud University) (submittedVersion)
Funders: KWF Kankerbestrijding
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords: p19ARF, p53, cellular senescence, proliferative arrest, RasV12, transcriptional repression, tumor suppressor signaling, senescence resistance
MeSH terms: Animals, Cell Division, DNA-Binding Proteins, Fibroblasts, Models, Genetic, Promoter Regions, Genetic, Proto-Oncogene Proteins, Genes, ras, Suppression, Genetic, Transcription Factors, Signal Transduction, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, 3T3 Cells, Cellular Senescence, Sequence Deletion, Cell Cycle Proteins, Cyclin-Dependent Kinase Inhibitor p16, Tumor Suppressor Protein p14ARF, E2F Transcription Factors, Mice

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E2F transcriptional repressor complexes are critical downstream targets of p19ARF/p53-induced proliferative arrest

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