Evidence map›Paper›PMID 26165517›Full record

ArticleeLife2015

Paracrine Met signaling triggers epithelial-mesenchymal transition in mammary luminal progenitors, affecting their fate.

Amandine Di-Cicco, Valérie Petit, Aurélie Chiche, Laura Bresson, Mathilde Romagnoli, Véronique Orian-Rousseau, Maria dM Vivanco, Daniel Medina, Marisa M Faraldo, Marina A Glukhova and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. 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
1.1field-weighted citation impact, top 20% 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, 27 citations in OpenAlex.

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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 7 institutions in 4 countries.

Amandine Di-CiccoInstitut Curie, Paris Sciences et Lettres Research University, Paris, France.
Valérie PetitInstitut Curie, Paris Sciences et Lettres Research University, Paris, France.
Aurélie ChicheInstitut Curie, Paris Sciences et Lettres Research University, Paris, France.
Laura BressonInstitut Curie, Paris Sciences et Lettres Research University, Paris, France.
Mathilde RomagnoliInstitut Curie, Paris Sciences et Lettres Research University, Paris, France.
Véronique Orian-RousseauKarlsruhe Institute of Technology, Karlsruhe, Germany.
Maria dM VivancoCell Biology and Stem Cells Unit, CIC bioGUNE, Derio, Spain.
Daniel MedinaBaylor College of Medicine, Houston, United States.
Marisa M FaraldoInstitut Curie, Paris Sciences et Lettres Research University, Paris, France.
Marina A GlukhovaInstitut Curie, Paris Sciences et Lettres Research University, Paris, France.
Marie-Ange DeugnierInstitut Curie, Paris Sciences et Lettres Research University, Paris, France.
Institut Curie · FRBiologie cellulaire et Cancer · FRLa Ligue Contre le Cancer · FRBaylor College of Medicine · USCIC bioGUNE · ESKarlsruhe Institute of Technology · DEUniversité Paris Sciences et Lettres · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HGF/Met signaling has recently been associated with basal-type breast cancers, which are thought to originate from progenitor cells residing in the luminal compartment of the mammary epithelium. We found that ICAM-1 efficiently marks mammary luminal progenitors comprising hormone receptor-positive and receptor-negative cells, presumably ductal and alveolar progenitors. Both cell populations strongly express Met, while HGF is produced by stromal and basal myoepithelial cells. We show that persistent HGF treatment stimulates the clonogenic activity of ICAM1-positive luminal progenitors, controlling their survival and proliferation, and leads to the expression of basal cell characteristics, including stem cell potential. This is accompanied by the induction of Snai1 and Snai2, two major transcription factors triggering epithelial-mesenchymal transition, the repression of the luminal-regulatory genes Elf5 and Hey1, and claudin down-regulation. Our data strongly indicate that paracrine Met signaling can control the function of luminal progenitors and modulate their fate during mammary development and tumorigenesis.

Indexed as

Epithelial-Mesenchymal TransitionParacrine CommunicationSignal TransductionAnimalsCells, CulturedEpithelial CellsHepatocyte Growth FactorMiceProto-Oncogene Proteins c-metStem CellsHepatocyte Growth FactorHGF protein, mouseHGFR protein, mouseProto-Oncogene Proteins c-metdevelopmental biologyepithelial–mesenchymal transitionICAM-1mammary glandMet signalingmousestem cells

Identifiers

PMID26165517
PMCPMC4498445
OpenAlexW2162714959

What OpenQuestion holds

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LicenceCC BY
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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.