Evidence map›Paper›PMID 22887998›Full record

ArticleThe Journal of biological chemistry2012

Tp53-induced glycolysis and apoptosis regulator (TIGAR) protects glioma cells from starvation-induced cell death by up-regulating respiration and improving cellular redox homeostasis.

Christina Wanka, Joachim P Steinbach, Johannes Rieger

Registry-linked trialOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07450833 (Assessing the Safety, Tolerability and Pharmacokinetics of Benfo-Oxythiamine), which is not on this map. Cited by 93 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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.

NCT07450833 phase1completednot on this mapstarted 2022, after this paper: background citation

Assessing the Safety, Tolerability and Pharmacokinetics of Benfo-Oxythiamine (B-OT) in Healthy Volunteers - An Open Label, Phase I Study

TypeinterventionalSponsorBenfovir AGRan2022 to 2022Enrolled48ConditionsHealthy VolunteersArmsBenfo-oxythiamine
3 · Its place in the literature

Who cites it

93 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Regulation of ROS signaling by TIGAR induces cancer-modulating responses in the tumor microenvironment.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. The role of TIGAR in nervous system diseases.Frontiers in aging neuroscience · 2022
    Review
  18. Review
  19. Review
  20. Review

33 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

3 authors at 2 institutions in 1 country.

Christina WankaDr. Senckenberg Institute of Neurooncology, Goethe University Frankfurt, Frankfurt, Germany.
Joachim P Steinbach
Johannes Rieger
Senckenberg Research Institute and Natural History Museum Frankfurt/M · DEGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered metabolism in tumor cells is increasingly recognized as a core component of the neoplastic phenotype. Because p53 has emerged as a master metabolic regulator, we hypothesized that the presence of wild-type p53 in glioblastoma cells could confer a selective advantage to these cells under the adverse conditions of the glioma microenvironment. Here, we report on the effects of the p53-dependent effector Tp53-induced glycolysis and apoptosis regulator (TIGAR) on hypoxia-induced cell death. We demonstrate that TIGAR is overexpressed in glioblastomas and that ectopic expression of TIGAR reduces cell death induced by glucose and oxygen restriction. Metabolic analyses revealed that TIGAR inhibits glycolysis and promotes respiration. Further, generation of reactive oxygen species (ROS) levels was reduced whereas levels of reduced glutathione were elevated in TIGAR-expressing cells. Finally, inhibiting the transketolase isoenzyme transketolase-like 1 (TKTL1) by siRNA reversed theses effects of TIGAR. These findings suggest that glioma cells benefit from TIGAR expression by (i) improving energy yield from glucose via increased respiration and (ii) enhancing defense mechanisms against ROS. Targeting metabolic regulators such as TIGAR may therefore be a valuable strategy to enhance glioma cell sensitivity toward spontaneously occurring or therapy-induced starvation conditions or ROS-inducing therapeutic approaches.

Indexed as

Gene Expression RegulationAnimalsApoptosisApoptosis Regulatory ProteinsBrain NeoplasmsCell DeathCell LineCell Line, TumorGene Expression Regulation, NeoplasticGliomaGlycolysisHumansHypoxiaIntracellular Signaling Peptides and ProteinsMiceModels, BiologicalApoptosis Regulatory ProteinsIntracellular Signaling Peptides and ProteinsPhosphoric Monoester HydrolasesReactive Oxygen SpeciesTIGAR protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22887998
PMCPMC3460445
OpenAlexW1984543978

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.