Evidence map›Paper›PMID 20154722›Full record

ArticleOncogene2010

Cyclin D1 is a direct transcriptional target of GATA3 in neuroblastoma tumor cells.

J J Molenaar, M E Ebus, J Koster, E Santo, D Geerts, R Versteeg, H N Caron

Open access · bronzeAbstract 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
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  4. A Novel Role for GATA3 in Mesangial Cells in Glomerular Development and Injury.Journal of the American Society of Nephrology : JASN · 2019
    Article
  5. Article
  6. Article
  7. Oncotarget · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
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  14. Article
  15. Article
  16. Article
  17. Gata3/Ruvbl2 complex regulates T helper 2 cell proliferation via repression of Cdkn2c expression.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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

7 authors at 2 institutions in 1 country.

J J MolenaarDepartment of Human Genetics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. j.j.molenaar@amc.uva.nl
M E Ebus
J Koster
E Santo
D Geerts
R Versteeg
H N Caron
Academic Medical Center · NLUniversity of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Almost all neuroblastoma tumors express excess levels of Cyclin D1 (CCND1) compared to normal tissues and other tumor types. Only a small percentage of these neuroblastoma tumors have high-level amplification of the Cyclin D1 gene. The other neuroblastoma tumors have equally high Cyclin D1 expression without amplification. Silencing of Cyclin D1 expression was previously found to trigger differentiation of neuroblastoma cells. Overexpression of Cyclin D1 is therefore one of the most frequent mechanisms with a postulated function in neuroblastoma pathogenesis. The cause for the Cyclin D1 overexpression is unknown. Here we show that Cyclin D1 overexpression results from transcriptional upregulation. To identify upstream regulators, we searched in mRNA profiles of neuroblastoma tumor series for transcription factors with expression patterns correlating to Cyclin D1. GATA3 most consistently correlated to Cyclin D1 in four independent data sets. We identified a highly conserved GATA3 binding site 27 bp upstream of the Cyclin D1 transcriptional start. Chromatin immune precipitation confirmed binding of GATA3 to the Cyclin D1 promoter. Overexpression of GATA3 induced Cyclin D1 promoter activity, which decreased after site-directed mutagenesis of the GATA3 binding site in the Cyclin D1 promoter. Silencing of GATA3 resulted in reduced Cyclin D1 promoter activity and reduced Cyclin D1 mRNA and protein levels. Moreover, GATA3 silencing caused differentiation that was similar to that caused by Cyclin D1 inhibition. These finding implicate GATA3 in Cyclin D1 overexpression in neuroblastoma.

Indexed as

Binding SitesCyclin D1GATA3 Transcription FactorGene Expression ProfilingHumansNeuroblastomaPromoter Regions, GeneticTranscription, GeneticCCND1 protein, humanCyclin D1GATA3 protein, humanGATA3 Transcription Factor

Identifiers

PMID20154722
OpenAlexW2001928210

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.