Evidence map›Paper›PMID 21042727›Full record

ArticleInternational journal of oncology2010

p53 Protects lung cancer cells against metabolic stress.

Chompunoot Sinthupibulyakit, Wanida Ittarat, William H St Clair, Daret K St Clair

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 52 citations in OpenAlex.

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  16. Bridge-Induced Translocation betweenFrontiers in oncology · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. Regulation of Cellular Metabolism and Hypoxia by p53.Cold Spring Harbor perspectives in medicine · 2016
    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

4 authors.

Chompunoot SinthupibulyakitGraduate Center for Toxicology, University of Kentucky, Lexington, KY 40536, USA.
Wanida Ittarat
William H St Clair
Daret K St Clair

Funding

Mechansins of MnSOD expression in normal and tumor cellsR01CA049797 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K · 1996 to 2014
$3.3M
Redox Modulation of Prostate CancerR01CA115801 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, WILLIAM H · 2007 to 2011
$1.3M
MECHANISM OF MNSOD EXPRESSION IN NORMAL &TUMOR CELLSR29CA049797 · NCI · WAKE FOREST UNIVERSITY · PI ST CLAIR, DARET K · 1990 to 1994
–
NCI NIH HHS CA049797NCI NIH HHS CA 115801NCI NIH HHS R01 CA049797NCI NIH HHS R01 CA115801
6 · The paper itself

Abstract

The preferential use of aerobic glycolysis for energy production by cancer cells, a phenomenon known as the 'Warburg effect', is well recognized and is being considered for therapeutic applications. However, whether inhibition of glycolysis will be effective in all types of cancer is unclear. The current study shows that a glycolytic inhibitor, 2-deoxy-D-glucose (2DG), exhibits the cytotoxic effect on non-small cell lung cancer in a p53-dependent manner. 2DG significantly inhibits ATP production in p53-deficient lung cancer cells (H358) but not in p53-wt cells (A549). In contrast to p53-wt cells, p53-defective cells are unable to compensate for their need of energy via oxidative phosphorylation (OXPHOS) when glycolysis is inhibited. In the presence of p53, increased ROS from OXPHOS increases the expression of p53 target genes known to modulate metabolism, including synthesis of cytochrome c oxidase 2 (SCO2) and TP53-induced glycolysis and apoptosis regulator (TIGAR). Importantly, 2DG selectively induces the expression of the antioxidant enzymes manganese superoxide dismutase (MnSOD) and glutathione peroxidase 1 (GPx1) in a p53-dependent manner. The results demonstrate that the killing of cancer cells by the inhibitor of glycolysis is more efficient in cancer cells without functional p53 and that p53 protects against metabolic stress by up-regulation of oxidative phosphorylation and modulation of antioxidants.

Indexed as

CytoprotectionAdaptation, PhysiologicalAdenosine TriphosphateAntioxidantsApoptosis Regulatory ProteinsCarcinoma, Non-Small-Cell LungCarrier ProteinsCell Line, TumorDeoxyglucoseHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsMitochondrial ProteinsMolecular ChaperonesOxidative PhosphorylationOxidative StressAdenosine TriphosphateAntioxidantsApoptosis Regulatory ProteinsCarrier ProteinsDeoxyglucoseIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsMolecular ChaperonesPhosphoric Monoester HydrolasesReactive Oxygen SpeciesSCO2 protein, humanTIGAR protein, humanTumor Suppressor Protein p53

Identifiers

PMID21042727
PMCPMC3086553
OpenAlexW2163513390

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.