Evidence map›Paper›PMID 17854498›Full record

ArticleBreast cancer research : BCR2007

BP1 transcriptionally activates bcl-2 and inhibits TNFalpha-induced cell death in MCF7 breast cancer cells.

Holly S Stevenson, Sidney W Fu, Joseph J Pinzone, Jinguen Rheey, Samuel J Simmens, Patricia E Berg

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

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  8. Anti-apoptotic effect of claudin-1 on TNF-α-induced apoptosis in human breast cancer MCF-7 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
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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 4 institutions in 1 country.

Holly S StevensonCenter for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, MD 20892, USA.
Sidney W Fu
Joseph J Pinzone
Jinguen Rheey
Samuel J Simmens
Patricia E Berg
George Washington University · USWashington University Medical Center · USCenter for Cancer Research · USThe Ohio State University · US

Funding

BP1 and Nuclear Hormone Signaling in Breast CancerK08CA101875 · NCI · OHIO STATE UNIVERSITY · PI PINZONE, JOSEPH J · 2003 to 2009
$710k
A Novel HOX Gene Target in Breast CancerR21CA091149 · NCI · GEORGE WASHINGTON UNIVERSITY · PI BERG, PATRICIA E · 2002 to 2003
$507k
Deregulated BP1 expression in breast carcinogenesisR03CA102928 · NCI · GEORGE WASHINGTON UNIVERSITY · PI FU, SIDNEY W · 2004 to 2005
$153k
NCI NIH HHS CA101875NCI NIH HHS CA102928NCI NIH HHS CA91149NCI NIH HHS K08 CA101875NCI NIH HHS R03 CA102928NCI NIH HHS R21 CA091149
6 · The paper itself

Abstract

introductionWe have previously shown that the Beta Protein 1 (BP1) homeodomain protein is expressed in 81% of invasive ductal breast carcinomas, and that increased BP1 expression correlates with tumor progression. The purpose of our current investigation was to determine whether elevated levels of BP1 in breast cancer cells are associated with increased cell survival.

methodsEffects on cell viability and apoptosis of MCF7 cells stably overexpressing BP1 were determined using MTT and Annexin V assays, and through examination of caspase activation. TNFalpha was used to induce apoptosis. The potential regulation of apoptosis-associated genes by BP1 was studied using real-time PCR and western blot analyses. Electrophoretic mobility shift assays, site-directed mutagenesis, and transient assays were performed to specifically characterize the interaction of BP1 with the promoter of the bcl-2 gene.

resultsStable overexpression of BP1 led to inhibition of apoptosis in MCF7 breast cancer cells challenged with TNFalpha. Increased BP1 resulted in reduced processing and activation of caspase-7, caspase-8, and caspase-9, and inactivation of the caspase substrate Poly(ADP-Ribose) Polymerase (PARP). Increased levels of full-length PARP and a decrease in procaspase-8 were also associated with BP1 overexpression. The bcl-2 gene is a direct target of BP1 since: (i) BP1 protein bound to a consensus binding sequence upstream of the bcl-2 P1 promoter in vitro. (ii) MCF7 cells overexpressing BP1 showed increased levels of bcl-2 mRNA and protein. (iii) Transient assays indicated that increased bcl-2 promoter activity is due to direct binding and modulation by BP1 protein. BP1 expression also prevented TNFalpha-mediated downregulation of bcl-2 mRNA and protein.

conclusionThese findings suggest mechanisms by which increased BP1 may impart a survival advantage to breast cancer cells, which could lead to increased resistance to therapeutic agents in patients.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticAnnexin A5ApoptosisBlotting, WesternBreast NeoplasmsCaspasesElectrophoretic Mobility Shift AssayGenetic VectorsHomeodomain ProteinsHumansLuciferasesMutagenesis, Site-DirectedPoly(ADP-ribose) PolymerasesPromoter Regions, GeneticProto-Oncogene Proteins c-bcl-2Annexin A5CaspasesDLX4 protein, humanHomeodomain ProteinsLuciferasesPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2Transcription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID17854498
PMCPMC2242656
OpenAlexW2163645436

What OpenQuestion holds

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LicenceCC BY
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.