Evidence map›Paper›PMID 30046386›Full record

ArticleOncotarget2018

The matrix protein Fibulin-3 promotes KISS1R induced triple negative breast cancer cell invasion.

Michelle M Noonan, Magdalena Dragan, Michael M Mehta, David A Hess, Muriel Brackstone, Alan B Tuck, Navin Viswakarma, Ajay Rana, Andy V Babwah, Frederic E Wondisford and 1 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 37% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Review
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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

11 authors at 4 institutions in 2 countries.

Michelle M NoonanDepartment of Physiology and Pharmacology, The University of Western Ontario, London, ON, Canada.
Magdalena DraganDepartment of Physiology and Pharmacology, The University of Western Ontario, London, ON, Canada.
Michael M MehtaDepartment of Physiology and Pharmacology, The University of Western Ontario, London, ON, Canada.
David A HessDepartment of Physiology and Pharmacology, The University of Western Ontario, London, ON, Canada.
Muriel BrackstoneDepartment of Oncology, The University of Western Ontario, London, ON, Canada.
Alan B TuckDepartment of Oncology, The University of Western Ontario, London, ON, Canada.
Navin ViswakarmaDepartment of Surgery, Division of Surgical Oncology, University of Illinois at Chicago, Chicago, IL, USA.
Ajay RanaDepartment of Surgery, Division of Surgical Oncology, University of Illinois at Chicago, Chicago, IL, USA.
Andy V BabwahDepartment of Pediatrics, Child Health Institute of NJ, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
Frederic E WondisfordDepartment of Medicine, Child Health Institute of NJ, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
Moshmi BhattacharyaDepartment of Physiology and Pharmacology, The University of Western Ontario, London, ON, Canada.
Western University · CARutgers, The State University of New Jersey · USUniversity of Illinois Chicago · USLawson Health Research Institute · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is a leading cause of cancer mortality. In particular, triple negative breast cancer (TNBC) comprise a heterogeneous group of basal-like tumors lacking estrogen receptor (ERα), progesterone receptor (PR) and HER2 (ErbB2). TNBC represents 15-20% of all breast cancers and occurs frequently in women under 50 years of age. Unfortunately, these patients lack targeted therapy, are typically high grade and metastatic at time of diagnosis. The mechanisms regulating metastasis remain poorly understood. We have previously shown that the kisspeptin receptor, KISS1R stimulates invasiveness of TNBC cells. In this report, we demonstrate that KISS1R signals via the secreted extracellular matrix protein, fibulin-3, to regulate TNBC invasion. We found that the fibulin-3 gene is amplified in TNBC primary tumors and that plasma fibulin-3 levels are elevated in TNBC patients compared to healthy subjects. In this study, we show that KISS1R activation increases fibulin-3 expression and secretion. We show that fibulin-3 regulates TNBC metastasis in a mouse experimental metastasis xenograft model and signals downstream of KISS1R to stimulate TNBC invasion, by activating matrix metalloproteinase 9 (MMP-9) and the MAPK pathway. These results identify fibulin-3 as a new downstream mediator of KISS1R signaling and as a potential biomarker for TNBC progression and metastasis, thus revealing KISS1R and fibulin-3 as novel drug targets in TNBC.

Indexed as

fibulin-3invasionkisspeptin receptormetastasistriple-negative breast cancer

Identifiers

PMID30046386
PMCPMC6059025
OpenAlexW2870958174

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.