Evidence map›Paper›PMID 15688035›Full record

ArticleOncogene2005

Cell-type-specific regulation of distinct sets of gene targets by Pax3 and Pax3/FKHR.

Salma Begum, Nashmil Emami, Nashmil Emani, Albert Cheung, Olivia Wilkins, Sandy Der, Paul A Hamel

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.8field-weighted citation impact, top 7% 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, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. A dysfunctional miR-1-TRPS1-MYOG axis drives ERMS by suppressing terminal myogenic differentiation.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Clinical Application of Prognostic Gene Expression Signature in Fusion Gene-Negative Rhabdomyosarcoma: A Report from the Children's Oncology Group.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. The endocannabinoid system and sex steroid hormone-dependent cancers.International journal of endocrinology · 2013
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
    Emani, Nashmil [corrected to Emami, Nashmil]
5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Salma BegumDepartment of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada M5S 1A8.
Nashmil Emami
Nashmil Emani
Albert Cheung
Olivia Wilkins
Sandy Der
Paul A Hamel
University of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The oncogenic fusion protein, Pax3/FKHR, is a more potent transcription factor relative to its normal counterpart, Pax3. Since Pax3 induced a mesenchymal to epithelial transition (MET) in human SaOS-2 osteosarcomas, we hypothesized that Pax3/FKHR would also induce a morphological change in SaOS-2 cells. We demonstrate here that Pax3/FKHR more potently induces a MET in SaOS-2 cells than Pax3. This greater potency was further evident where Pax3/FKHR, but not Pax3, induced a morphological alteration in U2-OS osteosarcoma cells. By microarray analysis, we determined that Pax3/FKHR altered the expression of gene targets in a manner quantitatively and qualitatively distinct from Pax3. Three classes of genes were identified: (i) genes induced or repressed by Pax3 and Pax3/FKHR, (ii) genes induced or repressed by Pax3/FKHR but not Pax3 and (iii) genes induced by Pax3/FKHR but repressed by Pax3. Chromatin immunoprecipitations confirmed the direct binding of Pax3/FKHR to the promoter region of several factors including cannabinoid receptor-1, EPHA2 and EPHA4. Verification of the microarray data also revealed coordinate alteration in the expression of factors involved in BMP4 signalling. Regulation of gene expression by Pax3 and Pax3/FKHR is, however, cell-type specific. BMP4 expression, for example, was repressed by both Pax3 and Pax3/FKHR in SaOS-2 cells, while in the rhabdomyosarcoma, RD, Pax3/FKHR, but not Pax3, induced BMP4 expression. Thus, our data reveal that Pax3/FKHR regulates a distinct but overlapping set of genes relative to Pax3 and that the global set of Pax3 and Pax3/FKHR gene targets is cell-type specific.

Indexed as

Gene Expression Regulation, Neoplastic5' Untranslated RegionsBone NeoplasmsCell Line, TumorDNA-Binding ProteinsDNA PrimersForkhead Box Protein O1Forkhead Transcription FactorsHumansOsteosarcomaPaired Box Transcription FactorsPAX3 Transcription FactorRecombinant Fusion ProteinsReverse Transcriptase Polymerase Chain ReactionRhabdomyosarcomaRNA, Neoplasm5' Untranslated RegionsDNA-Binding ProteinsDNA PrimersForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanPaired Box Transcription FactorsPAX3 protein, humanPAX3 Transcription FactorRecombinant Fusion ProteinsRNA, NeoplasmTranscription Factors

Identifiers

PMID15688035
OpenAlexW2042590114

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.