Cited by 600NF-κB Signaling PathwaysCancer-related Molecular PathwaysSignaling Pathways in Disease

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Transcriptional Cross Talk between NF-κB and p53

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Webster, Gill A., Perkins, Neil D.·1999·Molecular and Cellular Biology

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Abstract

Many cellular stimuli result in the induction of both the tumor suppressor p53 and NF-kappaB. In contrast to activation of p53, which is associated with the induction of apoptosis, stimulation of NF-kappaB has been shown to promote resistance to programmed cell death. These observations suggest that a regulatory mechanism must exist to integrate these opposing outcomes and coordinate this critical cellular decision-making event. Here we show that both p53 and NF-kappaB inhibit each other's ability to stimulate gene expression and that this process is controlled by the relative levels of each transcription factor. Expression of either wild-type p53 or the RelA(p65) NF-kappaB subunit suppresses stimulation of transcription by the other factor from a reporter plasmid in vivo. Moreover, endogenous, tumor necrosis factor alpha-activated NF-kappaB will inhibit endogenous wild-type p53 transactivation. Following exposure to UV light, however, the converse is observed, with p53 downregulating NF-kappaB-mediated transcriptional activation. Both p53 and RelA(p65) interact with the transcriptional coactivator proteins p300 and CREB-binding protein (CBP), and we demonstrate that these results are consistent with competition for a limiting pool of p300/CBP complexes in vivo. These observations have many implications for regulation of the transcriptional decision-making mechanisms that govern cellular processes such as apoptosis. Furthermore, they suggest a previously unrealized mechanism through which dysregulated NF-kappaB can contribute to tumorigenesis and disease.

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Authors: Webster, G. A., & Perkins, N. D.
Affiliations: University of Dundee (GB)
ORCID: Perkins, Neil D.
Venue: Molecular and Cellular Biology
Publisher: Informa UK Limited
Published: 1999-05-01
Volume: 19
Issue: 5
Pages: 3485-3495
ISSN: 0270-7306 (ISSN-L)
1098-5549
DOI: 10.1128/mcb.19.5.3485
PMC: PMC84141
OpenAlex: W2134542375
Cited by: 598
References: 87
Citations by year: 2026: 10 · 2025: 11 · 2024: 12 · 2023: 13 · 2022: 19 · 2021: 30 · 2020: 17 · 2019: 16 · 2018: 16 · 2017: 12 · 2016: 20 · 2015: 23 · 2014: 14 · 2013: 20 · 2012: 15
FWCI: 13.41
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Molecular and Cellular Biology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Royal Society
Tenovus
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords: NF-κB, p53, transcriptional crosstalk, RelA/p65, P300, CREB-binding protein, transcriptional coactivator, apoptosis, TNF-α, transcriptional repression, carcinogenesis
MeSH terms: Binding, Competitive, Cell Line, Gene Expression Regulation, Humans, Mutation, Repressor Proteins, Transcription, Genetic, Tumor Necrosis Factor-alpha, Ultraviolet Rays, Trans-Activators, Tumor Suppressor Protein p53, NF-kappa B, Apoptosis, Genes, Reporter, Transcription Factor RelA

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Transcriptional Cross Talk between NF-κB and p53

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