Evidence map›Paper›PMID 21761347›Full record

ArticleHormones & cancer2010

Estrogen-induced aurora kinase-A (AURKA) gene expression is activated by GATA-3 in estrogen receptor-positive breast cancer cells.

Shoulei Jiang, Hiroshi Katayama, Jin Wang, Sara Antonia Li, Yan Hong, Laszlo Radvanyi, Jonathan J Li, Subrata Sen

Abstract read
In one paragraph

Article in Hormones & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

25 citing papers in PubMed, 28 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Article
  5. Review
  6. Rat Models of Hormone Receptor-Positive Breast Cancer.Journal of mammary gland biology and neoplasia · 2024
    Review
  7. Article
  8. Review
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  11. Article
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  19. Prognosis value of mitotic kinase Aurora-A for primary duodenal adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    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

8 authors at 3 institutions in 1 country.

Shoulei JiangDepartment of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77054, USA.
Hiroshi Katayama
Jin Wang
Sara Antonia Li
Yan Hong
Laszlo Radvanyi
Jonathan J Li
Subrata Sen
The University of Texas MD Anderson Cancer Center · USUniversity of Kansas Medical Center · USUniversity of Kansas · US

Funding

Biomarkers for the Early Detection of Pancreatic CancerU01CA111302 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KILLARY, ANN M, SEN, SUBRATA · 2004 to 2015
$6.6M
Novel human oncogene STK15/BTAK/Aurora 2R01CA089716 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SEN, SUBRATA · 2001 to 2012
$2.3M
NCI NIH HHS R01 CA089716NCI NIH HHS R01CA089716NCI NIH HHS U01 CA111302NCI NIH HHS UO1CA111302
6 · The paper itself

Abstract

Aurora-A is a proto-oncogenic mitotic kinase that is frequently overexpressed in human epithelial malignancies including in breast and ovarian cancers. The mechanism of transcriptional upregulation of Aurora-A in human breast cancer is not yet elucidated. We report herein that Aurora-A transcription is positively regulated by GATA-3 in response to estrogen in estrogen receptor α (ERα)-positive cells. Transient expression of aurora-A promoter deletion mutants in luciferase constructs identified a GATA binding sequence motif as a functional regulatory element in ERα-positive breast cancer cells. Electrophoretic mobility shift assay identified the binding of regulatory proteins to the GATA element. Anti-GATA-3 antibody generated a supershifted complex. Recruitment of GATA-3 to the aurora-A promoter was verified by chromatin immunoprecipitation analysis with GATA-3 antibody. Ectopic expression of GATA-3 resulted in elevated expression of Aurora-A in both ERα-positive and negative cells while siRNA-mediated silencing led to downregulation of endogenous Aurora-A in ERα-positive cells. Estrogen treatment of ERα-positive cells induced increased Aurora-A expression with enhanced recruitment of GATA-3 to the aurora-A promoter. Finally, in the ACI rat model of estrogen-induced breast cancer, known to be associated with elevated Aurora-A expression, we observed increased expression of GATA-3 in preinvasive and invasive mammary epithelial cells exposed to prolonged estrogen treatment and in developing breast tumors. These results demonstrate a direct positive role of estrogen in regulating Aurora-A expression through activation of the ERα-GATA-3 signaling cascade and suggest that this pathway may be critical in the origin of estrogen-stimulated sporadic breast cancer.

Indexed as

AnimalsAurora Kinase AAurora KinasesBreast NeoplasmsCell Line, TumorFemaleGATA3 Transcription FactorGene ExpressionGene Expression Regulation, NeoplasticHumansPromoter Regions, GeneticProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyReceptors, EstrogenSignal TransductionAURKA protein, humanAurka protein, ratAurora Kinase AAurora KinasesGATA3 protein, humanGATA3 Transcription FactorProtein Serine-Threonine KinasesReceptors, Estrogen

Identifiers

PMID21761347
PMCPMC4501777
OpenAlexW2041575663

What OpenQuestion holds

Textmetadata
LicenceTDM
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.