Evidence map›Paper›PMID 20305691›Full record

ArticleOncogene2010

De-repression of CTGF via the miR-17-92 cluster upon differentiation of human glioblastoma spheroid cultures.

A Ernst, B Campos, J Meier, F Devens, F Liesenberg, M Wolter, G Reifenberger, C Herold-Mende, P Lichter, B Radlwimmer

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 2 pooled it
7.6field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 2 syntheses or guidelines pooled it, 146 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Heliyon · 2023
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Comprehensive Overview ofPathogens (Basel, Switzerland) · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Targeting Tumors Using Peptides.Molecules (Basel, Switzerland) · 2020
    Review

27 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

10 authors at 3 institutions in 2 countries.

A ErnstDivision of Molecular Genetics, German Cancer Research Center, Heidelberg, Germany.
B Campos
J Meier
F Devens
F Liesenberg
M Wolter
G Reifenberger
C Herold-Mende
P Lichter
B Radlwimmer
Heidelberg University · DEHeinrich Heine University Düsseldorf · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

All-trans retinoic acid is a potent promoter of cellular differentiation processes, which is used in cancer therapy. Glioblastoma spheroid cultures are enriched in tumor-initiating cells, and provide a model to test new treatment options in vitro. We investigated the molecular mechanisms of response to exposure to differentiation-promoting conditions in such cultures. Microarray analyses of five independent cultures showed that after induction of differentiation, inhibitors of transforming growth factor-beta/bone morphogenetic protein, Wnt/beta-catenin and IGF signaling were upregulated, whereas expression of several microRNAs decreased, particularly that of the miR-17-92 cluster. In primary astrocytic gliomas (n=82), expression of several members of miR-17-92 was significantly higher relative to those of normal brain (n=8) and significantly increased with tumor grade progression (P<0.05). A high-level amplification of the miR-17-92 locus was detected in one glioblastoma specimen. Transfection of inhibitors of miR-17-92 induced increased apoptosis and decreased cell proliferation in glioblastoma spheroids. Mir-17-92 inhibition was also associated with increased messenger RNA (mRNA) and/or protein expression of CDKN1A, E2F1, PTEN and CTGF. The CTGF gene was shown to be a target of miR-17-92 in glioblastoma spheroids by luciferase reporter assays. Our results suggest that miR-17-92 and its target CTGF mediate effects of differentiation-promoting treatment on glioblastoma cells through multiple regulatory pathways.

Indexed as

Apoptosis Regulatory ProteinsBcl-2-Like Protein 11Brain NeoplasmsCell DifferentiationCell ProliferationCell SurvivalConnective Tissue Growth FactorCpG IslandsCyclin-Dependent Kinase Inhibitor p21DNA MethylationE2F1 Transcription FactorGlioblastomaHumansMembrane ProteinsMicroRNAsProto-Oncogene ProteinsApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl-2-Like Protein 11CDKN1A protein, humanConnective Tissue Growth FactorCyclin-Dependent Kinase Inhibitor p21E2F1 protein, humanE2F1 Transcription FactorMembrane ProteinsMicroRNAsMIRN17 microRNA, humanProto-Oncogene ProteinsPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID20305691
OpenAlexW1963777304

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.