Evidence map›Paper›PMID 24141032›Full record

ArticleMolecular and cellular endocrinology2014

COUP-TFII inhibits NFkappaB activation in endocrine-resistant breast cancer cells.

Lacey M Litchfield, Savitri N Appana, Susmita Datta, Carolyn M Klinge

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Lacey M LitchfieldDepartment of Biochemistry & Molecular Biology, Center for Genetics and Molecular Medicine, University of Louisville School of Medicine, Louisville, KY 40292, USA.
Savitri N AppanaDeptartment of Bioinformatics and Biostatistics, University of Louisville School of Public Health and Information Sciences, Louisville, KY 40292, USA.
Susmita DattaDeptartment of Bioinformatics and Biostatistics, University of Louisville School of Public Health and Information Sciences, Louisville, KY 40292, USA.
Carolyn M KlingeDepartment of Biochemistry & Molecular Biology, Center for Genetics and Molecular Medicine, University of Louisville School of Medicine, Louisville, KY 40292, USA. Electronic address: carolyn.klinge@louisville.edu.
University of Louisville · US

Funding

UOFL ENVIRONMENTAL HEALTH SCIENCES TRAINING PROGRAMT32ES011564 · NIEHS · UNIVERSITY OF LOUISVILLE · PI David W Hein, John Pierce Wise · 2004 to 2026
$7.1M
Identification of Proteins from Mass Spectrometry Data: A Statistical ApproachR15CA170091 · NCI · UNIVERSITY OF LOUISVILLE · PI KONG, MAIYING · 2013 to 2013
$464k
NCI NIH HHS R15 CA170091NIEHS NIH HHS T32 ES011564
6 · The paper itself

Abstract

Reduced COUP-TFII expression contributes to endocrine resistance in breast cancer cells. Endocrine-resistant breast cancer cells have higher NFkappa B (NFκB) activity and target gene expression. The goal of this study was to determine if COUP-TFII modulates NFκB activity. Endocrine-resistant LCC9 cells with low endogenous COUP-TFII displayed ∼5-fold higher basal NFκB activity than parental endocrine-sensitive MCF-7 breast cancer cells. Transient transfection of LCC9 cells with COUP-TFII inhibited NFκB activation and reduced NFκB target gene expression. COUP-TFII and NFκB were inversely correlated in breast cancer patient samples. Endogenous COUP-TFII coimmunoprecipitated with NFκB subunits RelB and NFκB1 in MCF-7 cells. COUP-TFII inhibited NFκB-DNA binding in vitro and impaired coactivator induced NFκB transactivation. LCC9 cells were growth-inhibited by an NFκB inhibitor and 4-hydroxytamoxifen compared to MCF-7 cells. Together these data indicate a novel role for COUP-TFII in suppression of NFκB activity and explain, in part, why decreased COUP-TFII expression results in an endocrine-resistant phenotype.

Indexed as

Breast NeoplasmsCOUP Transcription Factor IIDNA, NeoplasmDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHormonesHumansImidazolesMCF-7 CellsNF-kappa BPhosphorylationProtein BindingProtein SubunitsQuinoxalinesRNA, Messenger4(2'-aminoethyl)amino-1,8-dimethylimidazo(1,2-a)quinoxalineCOUP Transcription Factor IIDNA, NeoplasmHormonesImidazolesNF-kappa BProtein SubunitsQuinoxalinesRNA, MessengerTranscription Factor RelA4-hydroxytamoxifen4-OHTA20/TNFAIP3Antiestrogenschicken ovalbumin upstream promoter transcription factor IICOUP-TFIIDrug resistanceERαestrogen receptorICAM1IL6intercellular adhesion molecule 1interleukin 6 (IL6)NFκB/NFkappa Bnuclear factor κBNuclear receptorsqPCRquantitative real-time PCRREresponse elementselective estrogen receptor downregulatorselective estrogen receptor modulatorSERDSERMTAMtamoxifenTamoxifenTNFαTNFα-induced protein 3Transcription factorstumor necrosis factor

Identifiers

PMID24141032
PMCPMC5089806
OpenAlexW2088601708

What OpenQuestion holds

Textmetadata
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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.