Evidence map›Paper›PMID 18320068›Full record

ArticleNeoplasia (New York, N.Y.)2008

FK506 binding protein mediates glioma cell growth and sensitivity to rapamycin treatment by regulating NF-kappaB signaling pathway.

Wei Jiang, Simona Cazacu, Cunli Xiang, Jean C Zenklusen, Howard A Fine, Michael Berens, Brock Armstrong, Chaya Brodie, Tom Mikkelsen

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

49 citing papers in PubMed, 85 citations in OpenAlex.

  1. Trial
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  3. Review
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  5. Article
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  7. Article
  8. Article
  9. AmotL2, IQGAP1, and FKBP51 Scaffold Proteins in Glioblastoma Stem Cell Niches.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. The Many Faces of FKBP51.Biomolecules · 2019
    Review
  16. Article
  17. Article
  18. Article
  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

9 authors at 3 institutions in 1 country.

Wei JiangHermelin Brain Tumor Center, Department of Neurosurgery, Henry Ford Hospital, Detroit, MI 48202, USA.
Simona Cazacu
Cunli Xiang
Jean C Zenklusen
Howard A Fine
Michael Berens
Brock Armstrong
Chaya Brodie
Tom Mikkelsen
Henry Ford Hospital · USNational Institute of Neurological Disorders and Stroke · USTranslational Genomics Research Institute · US

Funding

A MULTI-USE GLIOMA BIOREPOSITORYR24CA095809 · NCI · HENRY FORD HEALTH SYSTEM · PI MIKKELSEN, TOM · 2002 to 2006
$886k
Intramural NIH HHSNCI NIH HHS CA095809NCI NIH HHS R24 CA095809
6 · The paper itself

Abstract

FK506 binding protein 5 (FKBP5) belongs to a family of immunophilins named for their ability to bind immunosuppressive drugs, also known as peptidyl-prolyl cis-trans isomerases, and also with chaperones to help protein folding. Using glioma cDNA microarray analysis, we found that FKBP5 was overexpressed in glioma tumors. This finding was further validated by real-time reverse transcription-polymerase chain reaction and Western blot analysis. The roles of FKBP5 in glioma cells were then examined. We found that cell growth was suppressed after FKBP5 expression was inhibited by short interfering RNA transfection and enhanced by FKBP5 overexpression. Electrophoretic mobility shift assay showed that nuclear factor-kappa B (NF-kappaB) and DNA binding was enhanced by FKBP5 overexpression. The expression level of I-kappa B alpha and phosphorylated NF-kappaB was regulated by the expression of FKBP5. These data suggest that FKBP5 is involved in NF-kappaB pathway activation in glioma cells. In addition, FKBP5 overexpression in rapamycin-sensitive U87 cells blocked the cells' response to rapamycin treatment, whereas rapamycin-resistant glioma cells, both PTEN-positive and -negative, were synergistically sensitive to rapamycin after FKBP5 was knocked down, suggesting that the FKBP5 regulates glioma cell response to rapamycin treatment. In conclusion, our study demonstrates that FKBP5 plays an important role in glioma growth and chemoresistance through regulating signal transduction of the NF-kappaB pathway.

Indexed as

Antibiotics, AntineoplasticApoptosisBrain NeoplasmsCell Line, TumorDrug Resistance, NeoplasmGliomaHumansNF-kappa BOligonucleotide Array Sequence AnalysisSignal TransductionSirolimusTacrolimus Binding Protein 5Tacrolimus Binding ProteinsAntibiotics, AntineoplasticNF-kappa BSirolimusTacrolimus Binding Protein 5Tacrolimus Binding Proteins

Identifiers

PMID18320068
PMCPMC2259453
OpenAlexW1797946869

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.