Evidence map›Paper›PMID 22782351›Full record

ArticleBritish journal of cancer2012

TIGAR induces p53-mediated cell-cycle arrest by regulation of RB-E2F1 complex.

E Madan, R Gogna, P Kuppusamy, M Bhatt, U Pati, A A Mahdi

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 60 citations in OpenAlex.

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  4. Gut microbes · 2025
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  11. The role of TIGAR in nervous system diseases.Frontiers in aging neuroscience · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. HIF-transcribed p53 chaperones HIF-1α.Nucleic acids research · 2019
    Article
  16. Article
  17. Article
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  19. Article
  20. Article
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

6 authors at 3 institutions in 2 countries.

E MadanDepartment of Biochemistry, Chhatrapati Shahuji Maharaj Medical University, Lucknow 226003, India.
R Gogna
P Kuppusamy
M Bhatt
U Pati
A A Mahdi
King George's Medical University · INJawaharlal Nehru University · INThe Ohio State University · US

Funding

Probes and Methods for Clinical OximetryR01EB004031 · NIBIB · OHIO STATE UNIVERSITY · PI KUPPUSAMY, PERIANNAN · 2004 to 2021
$7.1M
NIBIB NIH HHS R01 EB004031
6 · The paper itself

Abstract

backgroundp53 induces cell-cycle arrest and apoptosis in cancer cells and negatively regulates glycolysis via TIGAR. Glycolysis is crucial for cancer progression although TIGAR provides protection from reactive oxygen species and apoptosis. The relation between TIGAR-mediated inhibition of glycolysis and p53 tumour-suppressor activity is unknown.

methodsRT-PCR, western blot, luciferase and chromatin immunoprecipitation assays were used to study TIGAR gene regulation. Co-IPP was used to determine the role of TIGAR protein in regulating the protein-protein interaction between retinoblastoma (RB) and E2F1. MCF-7 tumour xenografts were utilised to study the role of TIGAR in tumour regression.

resultsOur study shows that TIGAR promotes p21-independent, p53-mediated G1-phase arrest in cancer cells. p53 activates the TIGAR promoter only in cells exposed to repairable doses of stress. TIGAR regulates the expression of genes involved in cell-cycle progression; suppresses synthesis of CDK-2, CDK-4, CDK-6, Cyclin D, Cyclin E and promotes de-phosphorylation of RB protein. RB de-phosphorylation stabilises the complex between RB and E2F1 thus inhibiting the entry of cell cycle from G1 phase to S phase.

conclusionTIGAR mediates de-phosphorylation of RB and stabilisation of RB-E2F1 complex thus delaying the entry of cells in S phase of the cell cycle. Thus, TIGAR inhibits proliferation of cancer cells and increases drug-mediated tumour regression by promoting p53-mediated cell-cycle arrest.

Indexed as

Apoptosis Regulatory ProteinsCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesE2F1 Transcription FactorG1 PhaseGene ExpressionGlycolysisHumansIntracellular Signaling Peptides and ProteinsKB CellsPhosphoric Monoester HydrolasesPhosphorylationProtein Interaction Domains and MotifsApoptosis Regulatory ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesE2F1 Transcription FactorIntracellular Signaling Peptides and ProteinsPhosphoric Monoester HydrolasesTamoxifenTIGAR protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22782351
PMCPMC3405207
OpenAlexW1995140801

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.