Evidence map›Paper›PMID 23574722›Full record

ArticleCell cycle (Georgetown, Tex.)2013

p63 regulates glutaminase 2 expression.

Arianna Giacobbe, Lucilla Bongiorno-Borbone, Francesca Bernassola, Alessandro Terrinoni, Elke Katrin Markert, Arnold J Levine, Zhaohui Feng, Massimilano Agostini, Lello Zolla, Alessandro Finazzi Agrò and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Metabolic changes during prostate cancer development and progression.Journal of cancer research and clinical oncology · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Emerging Roles of p53 Family Members in Glucose Metabolism.International journal of molecular sciences · 2018
    Review
  19. Article
  20. Targeting Glutamine Metabolism for Cancer Treatment.Biomolecules & therapeutics · 2018
    Review
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 8 institutions in 4 countries.

Arianna GiacobbeDepartment of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy.
Lucilla Bongiorno-Borbone
Francesca Bernassola
Alessandro Terrinoni
Elke Katrin Markert
Arnold J Levine
Zhaohui Feng
Massimilano Agostini
Lello Zolla
Alessandro Finazzi Agrò
Daniel A Notterman
Gerry Melino
Angelo Peschiaroli
University of Rome Tor Vergata · ITCenter for Systems Biology · USInstitute of Cell Biology and Neurobiology · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITPenn State Milton S. Hershey Medical Center · USRutgers Cancer Institute of New JerseyUniversità degli Studi della Tuscia · ITUniversity of Leicester · GB

Funding

Medical Research Council MC_U132670600Telethon GGP09133
6 · The paper itself

Abstract

The transcription factor p63 is critical for many biological processes, including development and maintenance of epidermal tissues and tumorigenesis. Here, we report that the TAp63 isoforms regulate cell metabolism through the induction of the mitochondrial glutaminase 2 (GLS2) gene both in primary cells and tumor cell lines. By ChIP analysis and luciferase assay, we confirmed that TAp63 binds directly to the p53/p63 consensus DNA binding sequence within the GLS2 promoter region. Given the critical role of p63 in epidermal differentiation, we have investigated the regulation of GLS2 expression during this process. GLS2 and TAp63 expression increases during the in vitro differentiation of primary human keratinocytes, and depletion of GLS2 inhibits skin differentiation both at molecular and cellular levels. We found that GLS2 and TAp63 expression are concomitantly induced in cancer cells exposed to oxidative stresses. siRNA-mediated depletion of GLS2 sensitizes cells to ROS-induced apoptosis, suggesting that the TAp63/GLS2 axis can be functionally important as a cellular antioxidant pathway in the absence of p53. Accordingly, we found that GLS2 is upregulated in colon adenocarcinoma. Altogether, our findings demonstrate that GLS2 is a bona fide TAp63 target gene, and that the TAp63-dependent regulation of GLS2 is important for both physiological and pathological processes.

Indexed as

AdenocarcinomaApoptosisCell DifferentiationCell Line, TumorColonic NeoplasmsCytoprotectionDNA DamageGlutaminaseHistone Deacetylase InhibitorsHumansKeratinocytesReactive Oxygen SpeciesSkinStress, PhysiologicalTranscription FactorsTumor Suppressor ProteinsGlutaminaseHistone Deacetylase InhibitorsReactive Oxygen SpeciesTP63 protein, humanTranscription FactorsTumor Suppressor Proteinscolon carcinomaglutaminolysisp63skin differentiation

Identifiers

PMID23574722
PMCPMC3674067
OpenAlexW2057512766

What OpenQuestion holds

Textmetadata
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.