Evidence map›Paper›PMID 23921636›Full record

ArticleNucleic acids research2013

A Common Docking Domain in Progesterone Receptor-B links DUSP6 and CK2 signaling to proliferative transcriptional programs in breast cancer cells.

Christy R Hagan, Todd P Knutson, Carol A Lange

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.7field-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

35 citing papers in PubMed, 49 citations in OpenAlex.

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  14. Progesterone Receptor Attenuates STAT1-Mediated IFN Signaling in Breast Cancer.Journal of immunology (Baltimore, Md. : 1950) · 2019
    Article
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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

3 authors at 2 institutions in 2 countries.

Christy R HaganDepartments of Medicine and Pharmacology, Cell Signaling Program; Masonic Cancer Center, University of Minnesota, Cancer Cardiology Research Building, 2231 6th Street SE, Minneapolis, MN 55455, USA.
Todd P Knutson
Carol A Lange
University of Minnesota · USToxicologie, Pharmacologie et Signalisation Cellulaire · FR

Funding

TRAINING GRANT IN MICROBIOLOGY/CANCER RESEARCHT32CA009138 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Scott M. Dehm · 1985 to 2026
$11.3M
Role of Phospho-Progesterone Receptors (PR) in Hormone Refractory Breast CancerR01CA159712 · NCI · UNIVERSITY OF MINNESOTA · PI LANGE, CAROL A · 2012 to 2016
$1.9M
CK2-dependent phosphorylation of Progesterone Receptors mediates proliferative siK99CA166643 · NCI · UNIVERSITY OF MINNESOTA · PI HAGAN, CHRISTY · 2012 to 2013
$190k
NCI NIH HHS 1K99CA166643-01NCI NIH HHS R01 CA159712NCI NIH HHS T32 CA009138
6 · The paper itself

Abstract

Progesterone receptors (PR) are transcription factors relevant to breast cancer biology. Herein, we describe an N-terminal common docking (CD) domain in PR-B, a motif first described in mitogen-activated protein kinases. Binding studies revealed PR-B interacts with dual-specificity phosphatase 6 (DUSP6) via the CD domain. Mutation of the PR-B CD domain (mCD) attenuated cell cycle progression and expression of PR-B target genes (including STAT5A and Wnt1); mCD PR-B failed to undergo phosphorylation on Ser81, a ck2-dependent site required for expression of these genes. PR-B Ser81 phosphorylation was dependent on binding with DUSP6 and required for recruitment of a transcriptional complex consisting of PR-B, DUSP6 and ck2 to an enhancer region upstream of the Wnt1 promoter. STAT5 was present at this site in the absence or presence of progestin. Furthermore, phospho-Ser81 PR-B was recruited to the STAT5A gene upon progestin treatment, suggestive of a feed-forward mechanism. Inhibition of JAK/STAT-signaling blocked progestin-induced STAT5A and Wnt1 expression. Our studies show that DUSP6 serves as a scaffold for ck2-dependent PR-B Ser81 phosphorylation and subsequent PR-B-specific gene selection in coordination with STAT5. Coregulation of select target genes by PR-B and STAT5 is likely a global mechanism required for growth promoting programs relevant to mammary stem cell biology and cancer.

Indexed as

Gene Expression Regulation, NeoplasticBreast NeoplasmsCasein Kinase IICell Line, TumorCell ProliferationDual Specificity Phosphatase 6Enhancer Elements, GeneticFemaleHumansJanus KinasesPhosphorylationProgestinsProtein Interaction Domains and MotifsReceptors, ProgesteroneSerineSignal TransductionCasein Kinase IIDual Specificity Phosphatase 6DUSP6 protein, humanJanus Kinasesprogesterone receptor BProgestinsReceptors, ProgesteroneSerineSTAT5 Transcription FactorSTAT Transcription FactorsWnt1 Protein

Identifiers

PMID23921636
PMCPMC3799453
OpenAlexW2004795545

What OpenQuestion holds

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LicenceCC BY-NC
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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.