Evidence map›Paper›PMID 15592518›Full record

ArticleOncogene2005

SP100 inhibits ETS1 activity in primary endothelial cells.

John S Yordy, Omar Moussa, Huiping Pei, Damien Chaussabel, Runzhao Li, Dennis K Watson

Abstract 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. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

24 citing papers in PubMed, 50 citations in OpenAlex.

  1. Programmable ZBTB7A RNA NMolecular cancer · 2026
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  8. Article
  9. In the Tumor Microenvironment, ETS1 Is an Oncogenic Immune Protein: An Integrative Pancancer Analysis.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  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

6 authors at 3 institutions in 1 country.

John S YordyDepartment of Pathology and Laboratory Medicine, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Omar Moussa
Huiping Pei
Damien Chaussabel
Runzhao Li
Dennis K Watson
MUSC Hollings Cancer Center · USMedical University of South Carolina · USBaylor University · US

Funding

THE ROLE OF FLI1 IN CELLULAR DIFFERENTIATION AND DEVELOPMENTP01CA078582 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1998 to 2009
$9.1M
NCI NIH HHS P01CA78582
6 · The paper itself

Abstract

SP100 was first identified as a nuclear autoimmune antigen and is a constituent of the nuclear body. SP100 interacts with the ETS1 transcription factor, and we have previously shown that SP100 reduces ETS1-DNA binding and inhibits ETS1 transcriptional activity on the MMP1 and uPA promoters. We now demonstrate that SP100 expression is upregulated by interferons, which have been shown to be antiangiogenic, in primary endothelial cells. As ETS1 is functionally important in promoting angiogenesis, we tested the hypothesis that ETS1 activity is negatively modulated by SP100 in endothelial cells. SP100 directly antagonizes ETS1-mediated morphological changes in human umbilical vein endothelial cell (HUVEC) network formation and reduces HUVEC migration and invasion. To further understand the functional relationship between ETS1 and SP100, cDNA microarray analysis was utilized to assess reprogramming of gene expression by ETS1 and SP100. A subset of the differentially regulated genes, including heat-shock proteins (HSPs) H11, HSPA1L, HSPA6, HSPA8, HSPE1 and AXIN1, BRCA1, CD14, CTGF (connective tissue growth factor), GABRE (gamma-aminobutyric acid A receptor epsilon), ICAM1, SNAI1, SRD5A1 (steroid-5-alpha-reductase 1) and THY1, were validated by real-time PCR and a majority showed reciprocal expression in response to ETS1 and SP100. Interestingly, genes that are negatively regulated by ETS1 and upregulated by SP100 have antimigratory or antiangiogenic properties. Collectively, these data indicate that SP100 negatively modulates ETS1-dependent downstream biological processes.

Indexed as

Antigens, NuclearAutoantigensBase SequenceCell DivisionCell MovementCells, CulturedDNA PrimersEndothelium, VascularHumansNuclear ProteinsOligonucleotide Array Sequence AnalysisProto-Oncogene Protein c-ets-1Proto-Oncogene ProteinsProto-Oncogene Proteins c-etsTranscription FactorsUmbilical VeinsAntigens, NuclearAutoantigensDNA PrimersETS1 protein, humanNuclear ProteinsProto-Oncogene Protein c-ets-1Proto-Oncogene ProteinsProto-Oncogene Proteins c-etsSP100 protein, humanTranscription Factors

Identifiers

PMID15592518
OpenAlexW2066217969

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.