Evidence map›Paper›PMID 25514460›Full record

ArticleOncotarget2014

TAp73 promotes anabolism.

Ivano Amelio, Alexey A Antonov, Maria Valeria Catani, Renato Massoud, Francesca Bernassola, Richard A Knight, Gerry Melino, Alessandro Rufini

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. 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
1.6field-weighted citation impact, top 19% 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, 39 citations in OpenAlex.

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  11. Cancer predictive studies.Biology direct · 2020
    Review
  12. Regulation of Adult Neurogenesis in Mammalian Brain.International journal of molecular sciences · 2020
    Review
  13. Article
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  17. Luteolin-7-International journal of molecular sciences · 2019
    Article
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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.

Ivano AmelioMedical Research Council, Toxicology Unit, Leicester University, Leicester LE1 9HN, UK.
Alexey A AntonovMedical Research Council, Toxicology Unit, Leicester University, Leicester LE1 9HN, UK.
Maria Valeria CataniBiochemistry Laboratory, IDI-IRCCS, University of Rome Tor Vergata, Rome 00133, Italy.
Renato MassoudBiochemistry Laboratory, IDI-IRCCS, University of Rome Tor Vergata, Rome 00133, Italy.
Francesca BernassolaBiochemistry Laboratory, IDI-IRCCS, University of Rome Tor Vergata, Rome 00133, Italy.
Richard A KnightMedical Research Council, Toxicology Unit, Leicester University, Leicester LE1 9HN, UK.
Gerry MelinoMedical Research Council, Toxicology Unit, Leicester University, Leicester LE1 9HN, UK. Biochemistry Laboratory, IDI-IRCCS, University of Rome Tor Vergata, Rome 00133, Italy. Molecular Pharmacology Laboratory, Technological University, St-Petersburg, Russia.
Alessandro RufiniMedical Research Council, Toxicology Unit, Leicester University, Leicester LE1 9HN, UK. Department of Cancer Studies, Cancer Research UK, Leicester Centre, University of Leicester, Leicester, LE1 7RH, UK.
Medical Research Council · GBIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic adaptation has emerged as a hallmark of cancer and a promising therapeutic target, as rapidly proliferating cancer cells adapt their metabolism increasing nutrient uptake and reorganizing metabolic fluxes to support biosynthesis. The transcription factor p73 belongs to the p53-family and regulates tumorigenesis via its two N-terminal isoforms, with (TAp73) or without (ΔNp73) a transactivation domain. TAp73 acts as tumor suppressor, at least partially through induction of cell cycle arrest and apoptosis and through regulation of genomic stability. Here, we sought to investigate whether TAp73 also affects metabolic profiling of cancer cells. Using high throughput metabolomics, we unveil a thorough and unexpected role for TAp73 in promoting Warburg effect and cellular metabolism. TAp73-expressing cells show increased rate of glycolysis, higher amino acid uptake and increased levels and biosynthesis of acetyl-CoA. Moreover, we report an extensive TAp73-mediated upregulation of several anabolic pathways including polyamine and synthesis of membrane phospholipids. TAp73 expression also increases cellular methyl-donor S-adenosylmethionine (SAM), possibly influencing methylation and epigenetics, and promotes arginine metabolism, suggestive of a role in extracellular matrix (ECM) modeling. In summary, our data indicate that TAp73 regulates multiple metabolic pathways that impinge on numerous cellular functions, but that, overall, converge to sustain cell growth and proliferation.

Indexed as

ApoptosisBone NeoplasmsCell Line, TumorCell ProliferationDNA-Binding ProteinsGlycolysisHumansMetabolismNuclear ProteinsOsteosarcomaTranscriptional ActivationTumor Protein p73Tumor Suppressor Proteinsdelta Np73 protein, humanDNA-Binding ProteinsNuclear ProteinsTP73 protein, humanTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID25514460
PMCPMC4350352
OpenAlexW1590075430

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.