Evidence map›Paper›PMID 23874775›Full record

ArticlePloS one2013

Transcription factor Ets1 cooperates with estrogen receptor α to stimulate estradiol-dependent growth in breast cancer cells and tumors.

Brian T Kalet, Sara R Anglin, Anne Handschy, Liza E O'Donoghue, Charles Halsey, Laura Chubb, Christopher Korch, Dawn L Duval

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. ETS-targeted therapy: can it substitute for MEK inhibitors?Clinical and translational medicine · 2017
    Review
  10. The Estrogen Receptor α-Cistrome Beyond Breast Cancer.Molecular endocrinology (Baltimore, Md.) · 2016
    Review
  11. Review
  12. Review
  13. MicroRNA expression profiles differentiate chronic pain condition subtypes.Translational research : the journal of laboratory and clinical medicine · 2015
    Article
  14. Article
  15. 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

8 authors at 2 institutions in 1 country.

Brian T KaletFlint Animal Cancer Center, Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado, United States of America.
Sara R Anglin
Anne Handschy
Liza E O'Donoghue
Charles Halsey
Laura Chubb
Christopher Korch
Dawn L Duval
Colorado State University · USUniversity of Colorado Cancer Center · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Signaling Mechanisms Regulating Pituitary Gene ExpressionR56DK070952 · NIDDK · COLORADO STATE UNIVERSITY · PI DUVAL, DAWN L · 2009 to 2010
$577k
NCI NIH HHS P30 CA046934NCI NIH HHS P30CA046934NIDDK NIH HHS R56 DK070952
6 · The paper itself

Abstract

The purpose of this study was to explore the role of transcription factor Ets1 in estrogen receptor α (ERα)-positive breast cancer progression. We expressed human Ets1 or empty vector in four human ERα-positive breast cancer cell lines and observed increased colony formation. Further examination of cellular responses in stable Ets1-expressing MCF7 clones displayed increased proliferation, migration, and invasion. Ets1-expressing MCF7 tumors grown in the mammary fat pads of nude mice exhibited increased rates of tumor growth (7.36±2.47 mm(3)/day) compared to control MCF7 tumors (2.52±1.70 mm(3)/day), but maintained their dependence on estradiol for tumor growth. Proliferation marker Ki-67 staining was not different between control and Ets1-expressing tumors, but Ets1-expressing tumors exhibited large necrotic centers and elevated apoptotic staining. Ets1 was shown to cooperate with ERα and the p160 nuclear receptor coactivator (NCOA/SRC) family to increase activation of a consensus estrogen response element luciferase reporter construct. Ets1-expressing MCF7 cells also exhibited elevated expression of the ERα target genes, progesterone receptor and trefoil factor 1. Using GST-pulldown assays, Ets1 formed stable complexes containing both ERα and p160 nuclear receptor coactivators. Taken together, these data suggest that the Ets1-dependent estradiol sensitization of breast cancer cells and tumors may be partially due to the ability of Ets1 to cooperate with ERα and nuclear receptor coactivators to stimulate transcriptional activity of estrogen-dependent genes.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationEstradiolEstrogen Receptor alphaFemaleGene ExpressionHumansKi-67 AntigenMCF-7 CellsMiceMultiprotein ComplexesPlatelet Endothelial Cell Adhesion Molecule-1Protein BindingEstradiolEstrogen Receptor alphaKi-67 AntigenMultiprotein ComplexesPlatelet Endothelial Cell Adhesion Molecule-1Proto-Oncogene Protein c-ets-1

Identifiers

PMID23874775
PMCPMC3706316
OpenAlexW2094283635

What OpenQuestion holds

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LicenceCC BY
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.