ArticleOncogene2010
Cross talk between stimulated NF-kappaB and the tumor suppressor p53.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
88 citing papers in PubMed, 151 citations in OpenAlex.
- Targeting senescent cells in aged adipose tissue induced by ovarian cancer with the NF-κB inhibitor quercetin and resveratrol impedes the growth and metastasis of ovarian cancer.Science China. Life sciences · 2026Article
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- Bypassing the guardian: regulated cell death pathways in p53-mutant cancers.Cellular & molecular biology letters · 2025Review
- Betulinic acid and obesity-related disorders.Frontiers in pharmacology · 2025Review
- A Fungicide, Fludioxonil, Formed the Polyploid Giant Cancer Cells and Induced Metastasis and Stemness in MDA-MB-231 Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2024Article
- Novel hydroxamic acid derivative induces apoptosis and constrains autophagy in leukemic cells.Journal of advanced research · 2024Article
- TP53 gain-of-function mutations promote osimertinib resistance via TNF-α-NF-κB signaling in EGFR-mutated lung cancer.NPJ precision oncology · 2024Article
- Mutant p53 gains oncogenic functions through a chromosomal instability-induced cytosolic DNA response.Nature communications · 2024Article
- Bisphenol-A Abrogates Proliferation and Differentiation of C2C12 Mouse Myoblasts via Downregulation of Phospho-P65 NF-Journal of toxicology · 2024Article
- DNp73 enhances tumor progression and immune evasion in multiple myeloma by targeting the MYC and MYCN pathways.Frontiers in immunology · 2024Article
- Tumor suppressor p53 mediates interleukin-6 expression to enable cancer cell evasion of genotoxic stress.Cell death discovery · 2023Article
- Review
- Identifying key multifunctional components shared by critical cancer and normal liver pathways via SparseGMM.Cell reports methods · 2023Article
- The role of p53 in anti-tumor immunity and response to immunotherapy.Frontiers in molecular biosciences · 2023Review
- Correlation of Before and After Invasive Breast Cancer Neoadjuvant Chemotherapy for NFkB, Cyclin D1, and Survivin Expression.Iranian journal of pathology · 2023Article
- Article
- Review
- Host tp53 mutation induces gut dysbiosis eliciting inflammation through disturbed sialic acid metabolism.Microbiome · 2022Article
- Insights on the NF-κB System Using Live Cell Imaging: Recent Developments and Future Perspectives.Frontiers in immunology · 2022Review
- Adaptive homeostasis and the p53 isoform network.EMBO reports · 2021Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor-kappaB (NF-kappaB) and p53 critically determine cancer development and progression. Defining the cross talk between these transcription factors can expand our knowledge on molecular mechanisms of tumorigenesis. Here, we show that induction of replicational stress activates NF-kappaB p65 and triggers its interaction with p53 in the nucleus. Experiments with knockout cells show that p65 and p53 are both required for enhanced NF-kappaB activity during S-phase checkpoint activation involving ataxia-telangiectasia mutated and checkpoint kinase-1. Accordingly, the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) also triggers formation of a transcriptionally active complex containing nuclear p65 and p53 on kappaB response elements. Gene expression analyses revealed that, independent of NF-kappaB activation in the cytosol, TNF-induced NF-kappaB-directed gene expression relies on p53. Hence, p53 is unexpectedly necessary for NF-kappaB-mediated gene expression induced by atypical and classical stimuli. Remarkably, data from gain- and loss-of function approaches argue that anti-apoptotic NF-kappaB p65 activity is constitutively evoked by a p53 hot-spot mutant frequently found in tumors. Our observations suggest explanations for the outstanding question why p53 mutations rather than p53 deletions arise in tumors of various origins.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.