Evidence map›Paper›PMID 23873029›Full record

ArticleOncogene2014

Functions of TAp63 and p53 in restraining the development of metastatic cancer.

E H Tan, J P Morton, P Timpson, P Tucci, G Melino, E R Flores, O J Sansom, K H Vousden, P A J Muller

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Detection of Oral Submucous Fibrosis at the Crossroads of Altering Nucleogeometry, Nuclear Spatial Distribution and Nuclear Molecular Abundance.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2025
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  13. The Regulation of Tumor Suppressor p63 by the Ubiquitin-Proteasome System.International journal of molecular sciences · 2016
    Review
  14. Article
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  20. Association of SIRT1 and tumor suppressor gene TAp63 expression in head and neck squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

9 authors at 3 institutions in 2 countries.

E H TanCancer Research UK Beatson Institute, Glasgow, UK.
J P MortonCancer Research UK Beatson Institute, Glasgow, UK.
P Timpson1] Cancer Research UK Beatson Institute, Glasgow, UK [2] The Garvan Institute of Medical Research, The Kinghorn Cancer Centre, Cancer Program, Sydney, Australia.
P Tucci1] Medical Research Council, Toxicology Unit, Leicester University, Leicester, UK [2] Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende (CS), Italy.
G Melino1] Medical Research Council, Toxicology Unit, Leicester University, Leicester, UK [2] Biochemistry Laboratory, Istituto Dermopatico dell'Immacolata, Istituto di Ricovero e Cura a Carattere Scientifico and University of Rome ,"Tor Vergata," Rome, Italy.
E R FloresDepartment of Biochemistry and Molecular Biology, Graduate School of Biomedical Sciences, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA.
O J SansomCancer Research UK Beatson Institute, Glasgow, UK.
K H VousdenCancer Research UK Beatson Institute, Glasgow, UK.
P A J MullerCancer Research UK Beatson Institute, Glasgow, UK.
Cancer Research UK Scotland Institute · GBMedical Research Council · GBThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Roles of p63 in regulation of miRNA and LincRNA targets in metastatic cancerR01CA160394 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FLORES, ELSA R · 2012 to 2015
$2.0M
Cancer Research UK 11650Cancer Research UK 12481Medical Research Council MC_U132670600NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA160394
6 · The paper itself

Abstract

Many tumours harbour mutations in the p53 tumour-suppressor gene that result in the expression of a mutant p53 protein. This mutant p53 protein has, in most cases, lost wild-type transcriptional activity and can also acquire novel functions in promoting invasion and metastasis. One of the mechanisms underlying these novel functions involves the ability of the mutant p53 to interfere with other transcription factors, including the p53 family protein TAp63. To investigate whether simultaneous depletion of both p53 and TAp63 can recapitulate the effect of mutant p53 expression in vivo, we used a mouse model of pancreatic cancer in which the expression of mutant p53 resulted in the rapid appearance of primary tumours and metastases. As shown previously, loss of one allele of wild-type (WT) p53 accelerated tumour development. A change of one WT p53 allele into mutant p53 did not further accelerate tumour development, but did promote the formation of metastasis. By contrast, loss of TAp63 did not significantly accelerate tumour development or metastasis. However, simultaneous depletion of p53 and TAp63 led to both rapid tumour development and metastatic potential, although the incidence of metastases remained lower than that seen in mutant p53-expressing tumours. TAp63/p53-null cells derived from these mice also showed an enhanced ability to scatter and invade in tissue culture as was observed in mutant p53 cells. These data suggest that depletion of TAp63 in a p53-null tumour can promote metastasis and recapitulate-to some extent-the consequences of mutant p53 expression.

Indexed as

AnimalsCell Line, TumorHumansMiceMutationNeoplasm MetastasisPancreatic NeoplasmsTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor ProteinsTP63 protein, humanTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID23873029
PMCPMC4181588
OpenAlexW2108005267

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.