Evidence map›Paper›PMID 20729916›Full record

ArticleOncogene2010

YAP dysregulation by phosphorylation or ΔNp63-mediated gene repression promotes proliferation, survival and migration in head and neck cancer subsets.

R Ehsanian, M Brown, H Lu, X P Yang, A Pattatheyil, B Yan, P Duggal, R Chuang, J Doondeea, S Feller and 3 more

Abstract read
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
2.3field-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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
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  12. Article
  13. Context-dependent roles of YAP/TAZ in stem cell fates and cancer.Cellular and molecular life sciences : CMLS · 2021
    Review
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1 more citing papers are in PubMed but not listed here.

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

13 authors at 5 institutions in 2 countries.

R EhsanianTumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892-1419, USA.
M Brown
H Lu
X P Yang
A Pattatheyil
B Yan
P Duggal
R Chuang
J Doondeea
S Feller
M Sudol
Z Chen
C Van Waes
National Institute on Deafness and Other Communication Disorders · USNational Institutes of Health · USIcahn School of Medicine at Mount Sinai · USMRC Weatherall Institute of Molecular Medicine · GBUniversity of Oxford · GB

Funding

Signal and Transcription Factor Network interactions in Head and Neck CancerZIADC000073 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI VAN WAES, CARTER · 2009 to 2022
$9.1M
Intramural NIH HHS ZIA DC000073PHS HHS Z1ADC-000073PHS HHS Z1ADC-000074
6 · The paper itself

Abstract

Overexpression of the Yes-associated protein (YAP), and TP53 family members ΔNp63 and p73, have been independently detected in subsets of head and neck squamous cell carcinomas (HNSCCs). YAP may serve as a nuclear cofactor with ΔNp63 and p73, but the functional role of YAP and their potential relationship in HNSCCs are unknown. In this study, we show that in a subset of HNSCC lines and tumors, YAP expression is increased but localized in the cytoplasm in association with increased AKT and YAP phosphorylation, and with decreased expression of ΔNp63 and p73. In another subset, YAP expression is decreased but detectable in the nucleus in association with lower AKT and YAP phosphorylation, and with increased ΔNp63 and p73 expression. Inhibiting AKT decreased serine-127 phosphorylation and enhanced nuclear translocation of YAP. ΔNp63 bound to the YAP promoter and suppressed its expression. Transfection of a YAP-serine-127-alanine phosphoacceptor-site mutant or ΔNp63 knockdown significantly increased nuclear YAP and cell death. Conversely, YAP knockdown enhanced cell proliferation, survival, migration and cisplatin chemoresistance. Thus, YAP function as a tumor suppressor may alternatively be dysregulated by AKT phosphorylation at serine-127 and cytoplasmic sequestration, or by transcriptional repression by ΔNp63, in different subsets of HNSCC. AKT and/or ΔNp63 are potential targets for enhancing YAP-mediated apoptosis and chemosensitivity in HNSCCs.

Indexed as

Active Transport, Cell NucleusCarcinoma, Squamous CellCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationCell SurvivalDrug Resistance, NeoplasmHead and Neck NeoplasmsHumansNuclear ProteinsPhosphorylationPromoter Regions, GeneticProto-Oncogene Proteins c-aktTissue Array AnalysisTrans-ActivatorsCell Cycle ProteinsNuclear ProteinsProto-Oncogene Proteins c-aktTP63 protein, humanTrans-ActivatorsTranscription FactorsTumor Suppressor ProteinsYY1AP1 protein, human

Identifiers

PMID20729916
PMCPMC2991596
OpenAlexW2004407173

What OpenQuestion holds

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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.