Evidence map›Paper›PMID 19036881›Full record

ArticleEndocrinology2009

Role of c-Myb during prolactin-induced signal transducer and activator of transcription 5a signaling in breast cancer cells.

Feng Fang, Michael A Rycyzyn, Charles V Clevenger

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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  14. Negative cross talk between NFAT1 and Stat5 signaling in breast cancer.Molecular endocrinology (Baltimore, Md.) · 2011
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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 1 institution in 1 country.

Feng FangDepartment of Pathology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois 60611, USA.
Michael A Rycyzyn
Charles V Clevenger
Northwestern University · US

Funding

Regulation of Stat Function in Breast CancerR01CA102682 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CLEVENGER, CHARLES V · 2003 to 2007
$1.3M
NCI NIH HHS R01 CA102682NCI NIH HHS R01CA-102682
6 · The paper itself

Abstract

Implicated in the pathogenesis of breast cancer, prolactin (PRL) mediates its function in part through the prolactin receptor (PRLr)-associated Janus kinase 2 (Jak2)/signal transducer and activator of transcription 5 (Stat5) signaling complex. To delineate the mechanisms of Stat5a regulation in breast cancer, transcription factor-transcription factor (TF-TF) array analysis was employed to identify associated transcriptional regulators. These analyses revealed a PRL-inducible association of Stat5a with the transcription factor and protooncogene c-Myb. Confirmatory co-immunoprecipitation studies using lysates from both T47D and MCF7 breast cancer cells revealed a PRL-inducible association between these transcription factors. Ectopic expression of c-Myb enhanced the PRL-induced expression from both composite and synthetic Stat5a-responsive luciferase reporters. Chromatin immunoprecipitation assays also revealed a PRL-inducible association between c-Myb and endogenous Stat5a-responsive CISH promoter, which was associated with an enhanced expression of CISH gene product at the RNA and protein levels. Small interfering RNA-mediated c-Myb knockdown impaired the PRL-induced mRNA expression of five Stat5-responsive genes. DNA binding-defective mutants of c-Myb, incapable of activating expression from a c-Myb-responsive reporter, maintained their ability to enhance a Stat5a-responsive reporter. At a cellular level, ectopic expression of c-Myb resulted in an increase in T47D proliferation. Taken together, these results indicate that c-Myb potentiates Stat5a-driven gene expression, possibly functioning as a Stat5a coactivator, in human breast cancer.

Indexed as

Cell Line, TumorCell ProliferationChromatin ImmunoprecipitationGene Expression Regulation, NeoplasticHumansImmunoprecipitationProlactinPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-mybReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingSignal TransductionSTAT5 Transcription FactorSuppressor of Cytokine Signaling ProteinsTumor Suppressor ProteinsProlactinProto-Oncogene Proteins c-mybRNA, Small InterferingSTAT5A protein, humanSTAT5 Transcription FactorSuppressor of Cytokine Signaling ProteinsTumor Suppressor Proteins

Identifiers

PMID19036881
PMCPMC2659289
OpenAlexW2077987105

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.