Evidence map›Paper›PMID 26011589›Full record

ArticleCancer biology & therapy2015

IRF-1 inhibits NF-κB activity, suppresses TRAF2 and cIAP1 and induces breast cancer cell specific growth inhibition.

Michaele J Armstrong, Michael T Stang, Ye Liu, Jin Yan, Eva Pizzoferrato, John H Yim

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 32% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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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

6 authors at 2 institutions in 1 country.

Michaele J Armstronga Department of Surgery; University of Pittsburgh School of Medicine ; Pittsburgh , PA , USA.
Michael T Stang
Ye Liu
Jin Yan
Eva Pizzoferrato
John H Yim
University of Pittsburgh · USCity Of Hope National Medical Center · US

Funding

Role of IRF-1 in Tumor Suppression of Breast CancerK08CA098403 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI YIM, JOHN H · 2004 to 2008
$660k
NCI NIH HHS CA098403
6 · The paper itself

Abstract

Interferon Regulatory Factor (IRF)-1, originally identified as a transcription factor of the human interferon (IFN)-β gene, mediates tumor suppression and may inhibit oncogenesis. We have shown that IRF-1 in human breast cancer cells results in the down-regulation of survivin, tumor cell death, and the inhibition of tumor growth in vivo in xenogeneic mouse models. In this current report, we initiate studies comparing the effect of IRF-1 in human nonmalignant breast cell and breast cancer cell lines. While IRF-1 in breast cancer cells results in growth inhibition and cell death, profound growth inhibition and cell death are not observed in nonmalignant human breast cells. We show that TNF-α or IFN-γ induces IRF-1 in breast cancer cells and results in enhanced cell death. Abrogation of IRF-1 diminishes TNF-α and IFN-γ-induced apoptosis. We test the hypothesis that IRF-1 augments TNF-α-induced apoptosis in breast cancer cells. Potential signaling networks elicited by IRF-1 are investigated by evaluating the NF-κB pathway. TNF-α and/or IFN-γ results in decreased presence of NF-κB p65 in the nucleus of breast cancer cells. While TNF-α and/or IFN-γ can induce IRF-1 in nonmalignant breast cells, a marked change in NF-κB p65 is not observed. Moreover, the ectopic expression of IRF-1 in breast cancer cells results in caspase-3, -7, -8 cleavage, inhibits NF-κB activity, and suppresses the expression of molecules involved in the NF-κB pathway. These data show that IRF-1 in human breast cancer cells elicits multiple signaling networks including intrinsic and extrinsic cell death and down-regulates molecules involved in the NF-κB pathway.

Indexed as

ApoptosisBreast NeoplasmsCaspasesCell LineCell Line, TumorCell ProliferationHumansImmunoblottingInhibitor of Apoptosis ProteinsInterferon-gammaInterferon Regulatory Factor-1NF-kappa BRNA InterferenceSignal TransductionTNF Receptor-Associated Factor 2Transcription Factor RelACaspasesInhibitor of Apoptosis ProteinsInterferon-gammaInterferon Regulatory Factor-1IRF1 protein, humanNF-kappa BTNF Receptor-Associated Factor 2Transcription Factor RelATumor Necrosis Factor-alphaAd, adenovirusapoptosisbreast cancerCdk, cyclin-dependent kinasecFLIP, cellular FLICE inhibitory proteincIAP1, c-inhibitor of apoptosisDISC, death-inducing signaling complexDMEM, Dulbecco's Modified Eagle's MediumDR, death receptorEGFP, enhanced green fluorescent proteinER, estrogen receptorFADD, fas-associated death domainFBS, Fetal Bovine SerumFITC, fluorescein isothiocyanateFLICE, fas-associated death domain protein interleukin-1 β-converting enzymeIAPIFN-β, interferon-βIFN-γ, interferon-gammaIKK, IκB, kinase complexIRF-1IRF-1, interferon regulatory factor-1IκB, Inhibitory kappaBMOI, multiplicity of infectionMTT, methylthiazoltetrazoliumNEMO, NF-κB essential modulatorNF-κBNF-κB, nuclear factor of kappa Betap53RIP1, receptor interacting protein 1SCID, severe combined immunodeficiencysiRNA, small interfering RNASmac/DIABLO, Second mitochondria-derived activator of caspase/Direct IAP-binding protein with low pISTAT, signal transducer and activator of transcriptionTNFR, tumor necrosis factor receptorTNF-α, tumor necrosis factor-αTRADD, TNF receptor associated protein with a death domainTRAF2, tumor necrosis factor receptor-associated factor 2TRAIL, tumor necrosis factor-related apoptosis-inducing ligandtumor suppressorXIAP, X-linked inhibitor of apoptosis proteinβ-gal, β-galactosidase

Identifiers

PMID26011589
PMCPMC4622679
OpenAlexW1546040549

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.