Evidence map›Paper›PMID 18593911›Full record

ArticleCancer research2008

The p53 homologue DeltaNp63alpha interacts with the nuclear factor-kappaB pathway to modulate epithelial cell growth.

Kathryn E King, Roshini M Ponnamperuma, Clint Allen, Hai Lu, Praveen Duggal, Zhong Chen, Carter Van Waes, Wendy C Weinberg

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.9field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. The dual role of p63 in cancer.Frontiers in oncology · 2023
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Molecular Mechanisms of p63-Mediated Squamous Cancer Pathogenesis.International journal of molecular sciences · 2019
    Review
  12. Article
  13. Inhibition of NF-Oncotarget · 2018
    Article
  14. STAT3, stem cells, cancer stem cells and p63.Cellular & molecular biology letters · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Kathryn E KingDivision of Monoclonal Antibodies, Center for Drug Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892, USA.
Roshini M Ponnamperuma
Clint Allen
Hai Lu
Praveen Duggal
Zhong Chen
Carter Van Waes
Wendy C Weinberg
National Institute on Deafness and Other Communication Disorders · USCenter for Drug Evaluation and Research · USNational Institutes of Health · US

Funding

NF-kappaB in pathogenesis and therapy of head and neck cancerZ01DC000016 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI VAN WAES, CARTER · 1994 to 2008
$2.9M
Signal and Transcription Factor Network interactions in Head and Neck CancerZ01DC000073 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI VAN WAES, CARTER · 2008 to 2008
$607k
Intramural NIH HHS Z01 DC000016
6 · The paper itself

Abstract

The p53 homologue DeltaNp63alpha is overexpressed and inhibits apoptosis in a subset of human squamous cell carcinomas (SCC). Here, we report that in normal keratinocytes overexpressing DeltaNp63alpha and in human squamous carcinoma cells, DeltaNp63alpha physically associates with phosphorylated, transcriptionally active nuclear c-Rel, a nuclear factor-kappaB family member, resulting in increased c-Rel nuclear accumulation. This accumulation and the associated enhanced proliferation driven by elevated DeltaNp63alpha are attenuated by c-Rel small interfering RNA or overexpression of mutant IkappaBalphaM, indicating that c-Rel-containing complex formation is critical to the ability of elevated DeltaNp63alpha to maintain proliferation in the presence of growth arresting signals. Consistent with a role in growth regulation, DeltaNp63alpha-c-Rel complexes bind a promoter motif and repress the cyclin-dependent kinase inhibitor p21WAF1 in both human squamous carcinoma cells and normal keratinocytes overexpressing DeltaNp63alpha. The relationship between DeltaNp63alpha and activated c-Rel is reflected in their strong nuclear staining in the proliferating compartment of primary head and neck SCC. This is the first report indicating that high levels of DeltaNp63alpha interact with activated c-Rel in keratinocytes and SCC, thereby promoting uncontrolled proliferation, a key alteration in the pathogenesis of cancers.

Indexed as

Cell ProliferationAnimalsCarcinoma, Squamous CellCells, CulturedEpithelial CellsHead and Neck NeoplasmsHumansKeratinocytesMiceMice, Inbred C57BLNF-kappa BProtein IsoformsProto-Oncogene Proteins c-relSequence HomologySignal TransductionTrans-ActivatorsNF-kappa BProtein IsoformsProto-Oncogene Proteins c-relTP63 protein, humanTrans-ActivatorsTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID18593911
PMCPMC2692507
OpenAlexW2139731426

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.