Evidence map›Paper›PMID 34749806›Full record

ReviewBiology direct2021

The p53 family member p73 in the regulation of cell stress response.

Julian M Rozenberg, Svetlana Zvereva, Aleksandra Dalina, Igor Blatov, Ilya Zubarev, Daniil Luppov, Alexander Bessmertnyi, Alexander Romanishin, Lamak Alsoulaiman, Vadim Kumeiko and 4 more

Open access · goldAbstract readReview
In one paragraph

Review in Biology direct, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
5.6field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. MicroRNA-21 Expression as a Prognostic Biomarker in Oral Cancer: Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2022
    Pooled it
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  14. Role of BRCA1 in glioblastoma etiology.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review
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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

14 authors at 6 institutions in 2 countries.

Julian M RozenbergCell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia. rozenbej@gmail.com.ORCID 0000-0002-7627-5217
Svetlana Zvereva *Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
Aleksandra Dalina *The Engelhardt Institute of Molecular Biology, Russian Academy of Science, Moscow, Russia.
Igor Blatov *Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
Ilya ZubarevCell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
Daniil LuppovCell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
Alexander BessmertnyiHSE University, Moscow, Russia.
Alexander RomanishinSchool of Biomedicine, Far Eastern Federal University, Vladivostok, Russia.
Lamak AlsoulaimanCell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
Vadim KumeikoSchool of Biomedicine, Far Eastern Federal University, Vladivostok, Russia.
Alexander KaganskyCell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
Gerry MelinoDepartment of Medicine, University of Rome Tor Vergata, Rome, Italy.
Carlo GaniniDepartment of Medicine, University of Rome Tor Vergata, Rome, Italy.
Nikolai A BarlevCell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia. nick.a.barlev@gmail.com.
Moscow Institute of Physics and Technology · RUUniversity of Rome Tor Vergata · ITEngelhardt Institute of Molecular Biology · RUFar Eastern Federal University · RUImmanuel Kant Baltic Federal University · RUNational Research University Higher School of Economics · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During oncogenesis, cells become unrestrictedly proliferative thereby altering the tissue homeostasis and resulting in subsequent hyperplasia. This process is paralleled by resumption of cell cycle, aberrant DNA repair and blunting the apoptotic program in response to DNA damage. In most human cancers these processes are associated with malfunctioning of tumor suppressor p53. Intriguingly, in some cases two other members of the p53 family of proteins, transcription factors p63 and p73, can compensate for loss of p53. Although both p63 and p73 can bind the same DNA sequences as p53 and their transcriptionally active isoforms are able to regulate the expression of p53-dependent genes, the strongest overlap with p53 functions was detected for p73. Surprisingly, unlike p53, the p73 is rarely lost or mutated in cancers. On the contrary, its inactive isoforms are often overexpressed in cancer. In this review, we discuss several lines of evidence that cancer cells develop various mechanisms to repress p73-mediated cell death. Moreover, p73 isoforms may promote cancer growth by enhancing an anti-oxidative response, the Warburg effect and by repressing senescence. Thus, we speculate that the role of p73 in tumorigenesis can be ambivalent and hence, requires new therapeutic strategies that would specifically repress the oncogenic functions of p73, while keeping its tumor suppressive properties intact.

Indexed as

DNA-Binding ProteinsGenes, Tumor SuppressorHumansNuclear ProteinsPhosphoproteinsTrans-ActivatorsTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor ProteinsDNA-Binding ProteinsNuclear ProteinsPhosphoproteinsTrans-ActivatorsTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor ProteinsCancer hallmarksp73Tumor suppressor p53

Identifiers

PMID34749806
PMCPMC8577020
OpenAlexW3213824183

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.