Evidence map›Paper›PMID 23378579›Full record

ArticleMolecular cancer research : MCR2013

The HER2- and heregulin β1 (HRG)-inducible TNFR superfamily member Fn14 promotes HRG-driven breast cancer cell migration, invasion, and MMP9 expression.

Kaushal Asrani, Ruth A Keri, Rebeca Galisteo, Sharron A N Brown, Sarah J Morgan, Arundhati Ghosh, Nhan L Tran, Jeffrey A Winkles

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.9field-weighted citation impact, top 5% 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, 41 citations in OpenAlex.

  1. Role of the MDM2/p53 axis in regulating cisplatin response in tumor cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  18. Generation of homologous cell pairs using the oral lymphatic system.International journal of clinical and experimental pathology · 2014
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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

8 authors at 4 institutions in 1 country.

Kaushal AsraniDepartment of Surgery, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Ruth A Keri
Rebeca Galisteo
Sharron A N Brown
Sarah J Morgan
Arundhati Ghosh
Nhan L Tran
Jeffrey A Winkles
Translational Genomics Research Institute · USUniversity of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer CenterCase Western Reserve University · USUniversity of Maryland, Baltimore · US

Funding

UNIVERSITY OF MARYLAND GREENEBAUM CANCER CENTERSUPPORT GRANTP30CA134274 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI FEYRUZ VIRGILIA RASSOOL · 2008 to 2026
$51.0M
Regulation of erbB2/Neu-induced mammary gland cancerR01CA090398 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI KERI, RUTH A. · 2001 to 2011
$2.7M
Targeting the Fn14-Rac1 signaling pathway in invasive gliomasR01CA130940 · NCI · TRANSLATIONAL GENOMICS RESEARCH INST · PI TRAN, NHAN L · 2008 to 2012
$1.5M
NCI NIH HHS P30 CA134274NCI NIH HHS R01 CA090398NCI NIH HHS R01 CA130940PHS HHS KG081095
6 · The paper itself

Abstract

HER2 overexpression occurs in 15% to 20% of all breast cancers and is associated with increased metastatic potential and poor patient survival. Abnormal HER2 activation, either through HER2 overexpression or heregulin (HRG):HER3 binding, elicits the formation of potent HER2-HER3 heterodimers and drives breast cancer cell growth and metastasis. In a previous study, we found that fibroblast growth factor-inducible 14 (Fn14), a member of the TNF receptor superfamily, was frequently overexpressed in human HER2+ breast tumors. We report here that HER2 and Fn14 are also coexpressed in mammary tumors that develop in two different transgenic mouse models of breast cancer. In consideration of these findings, we investigated whether HER2 activation in breast cancer cells could directly induce Fn14 gene expression. We found that transient or stable transfection of MCF7 cells with a HER2 expression plasmid increased Fn14 protein levels. Also, HRG1-β1 treatment of MCF7 cells transiently induced Fn14 mRNA and protein expression. Both the HER2- and HRG1-β1-induced increase in Fn14 expression in MCF7 cells as well as basal Fn14 expression in HER2 gene-amplified AU565 cells could be reduced by HER2 kinase inhibition with lapatinib or combined HER2 and HER3 depletion using siRNA. We also report that Fn14-depleted, HER2-overexpressing MCF7 cells have reduced basal cell migration capacity and reduced HRG1-β1-stimulated cell migration, invasion, and matrix metalloproteinase (MMP)-9 expression. Together, these results indicate that Fn14 may be an important downstream regulator of HER2/HER3-driven breast cancer cell migration and invasion.

Indexed as

AnimalsBreast NeoplasmsCell MovementDisease Models, AnimalErb-b2 Receptor Tyrosine KinasesFemaleHumansMaleMatrix Metalloproteinase 9MiceMice, TransgenicNeuregulin-1Receptors, Tumor Necrosis FactorTransfectionTWEAK ReceptorErb-b2 Receptor Tyrosine Kinasesheregulin beta1Matrix Metalloproteinase 9Neuregulin-1Receptors, Tumor Necrosis FactorTNFRSF12A protein, humanTnfrsf12a protein, mouseTWEAK Receptor

Identifiers

PMID23378579
PMCPMC3631278
OpenAlexW2331534532

What OpenQuestion holds

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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.