Evidence map›Paper›PMID 25926557›Full record

ArticleOncotarget2015

Organ-specific adaptive signaling pathway activation in metastatic breast cancer cells.

Riesa M Burnett, Kelly E Craven, Purna Krishnamurthy, Chirayu P Goswami, Sunil Badve, Peter Crooks, William P Mathews, Poornima Bhat-Nakshatri, Harikrishna Nakshatri

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

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  11. Gene-environment interaction identification via penalized robust divergence.Biometrical journal. Biometrische Zeitschrift · 2022
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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

9 authors at 3 institutions in 1 country.

Riesa M BurnettDepartment of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
Kelly E CravenDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Purna KrishnamurthyDepartment of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
Chirayu P GoswamiDepartment of Center for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN, USA.
Sunil BadveDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
Peter CrooksUniversity of Arkansas, Little Rock, AR, USA.
William P MathewsLeuchemix, Inc., Woodside, CA, USA.
Poornima Bhat-NakshatriDepartment of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
Harikrishna NakshatriDepartment of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USUniversity of Arkansas at Little Rock · US

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Jun Wan · 1999 to 2026
$59.3M
Indiana Medical Scientist/Engineer Training ProgramT32GM077229 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI GASTON, BENJAMIN, HERBERT, BRITTNEY-SHEA · 2008 to 2022
$6.0M
Cancer Biology Training ProgramT32CA111198 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI NAKSHATRI, HARIKRISHNA · 2005 to 2009
$1.8M
NCI NIH HHS CA111198NCI NIH HHS P30 CA082709NCI NIH HHS T32 CA111198NIGMS NIH HHS 5T32GM77229-5NIGMS NIH HHS T32 GM077229
6 · The paper itself

Abstract

Breast cancer metastasizes to bone, visceral organs, and/or brain depending on the subtype, which may involve activation of a host organ-specific signaling network in metastatic cells. To test this possibility, we determined gene expression patterns in MDA-MB-231 cells and its mammary fat pad tumor (TMD-231), lung-metastasis (LMD-231), bone-metastasis (BMD-231), adrenal-metastasis (ADMD-231) and brain-metastasis (231-BR) variants. When gene expression between metastases was compared, 231-BR cells showed the highest gene expression difference followed by ADMD-231, LMD-231, and BMD-231 cells. Neuronal transmembrane proteins SLITRK2, TMEM47, and LYPD1 were specifically overexpressed in 231-BR cells. Pathway-analyses revealed activation of signaling networks that would enable cancer cells to adapt to organs of metastasis such as drug detoxification/oxidative stress response/semaphorin neuronal pathway in 231-BR, Notch/orphan nuclear receptor signals involved in steroidogenesis in ADMD-231, acute phase response in LMD-231, and cytokine/hematopoietic stem cell signaling in BMD-231 cells. Only NF-κB signaling pathway activation was common to all except BMD-231 cells. We confirmed NF-κB activation in 231-BR and in a brain metastatic variant of 4T1 cells (4T1-BR). Dimethylaminoparthenolide inhibited NF-κB activity, LYPD1 expression, and proliferation of 231-BR and 4T1-BR cells. Thus, transcriptome change enabling adaptation to host organs is likely one of the mechanisms associated with organ-specific metastasis and could potentially be targeted therapeutically.

Indexed as

TranscriptomeBreast NeoplasmsCell Line, TumorElectrophoretic Mobility Shift AssayFemaleGene Expression Regulation, NeoplasticHumansNeoplasm MetastasisOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionSignal Transductionbrain metastasisbreast cancerDMAPTNF-kBTMEM47

Identifiers

PMID25926557
PMCPMC4494966
OpenAlexW1884264718

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.