Evidence map›Paper›PMID 30065298›Full record

ArticleOncogene2018

Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function.

Alessia Castagnino, Antonio Castro-Castro, Marie Irondelle, Alan Guichard, Catalina Lodillinsky, Laetitia Fuhrmann, Sophie Vacher, Sonia Agüera-González, Anna Zagryazhskaya-Masson, Maryse Romao and 9 more

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In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Genes · 2023
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  7. Article
  8. Article
  9. Review
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  13. Article
  14. Tissue remodeling by invadosomes.Faculty reviews · 2021
    Review
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  16. Review
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  18. Article
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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

19 authors at 5 institutions in 4 countries.

Alessia CastagninoInstitut Curie, PSL Research University, CNRS UMR144, Membrane and Cytoskeleton Dynamics group, 26 rue d'Ulm, F-75005, Paris, France.
Antonio Castro-CastroInstitut Curie, PSL Research University, CNRS UMR144, Membrane and Cytoskeleton Dynamics group, 26 rue d'Ulm, F-75005, Paris, France.
Marie IrondelleInstitut Curie, PSL Research University, CNRS UMR144, Membrane and Cytoskeleton Dynamics group, 26 rue d'Ulm, F-75005, Paris, France.
Alan GuichardInstitut Curie, PSL Research University, CNRS UMR144, Membrane and Cytoskeleton Dynamics group, 26 rue d'Ulm, F-75005, Paris, France.
Catalina LodillinskyInstitut Curie, PSL Research University, CNRS UMR144, Membrane and Cytoskeleton Dynamics group, 26 rue d'Ulm, F-75005, Paris, France.
Laetitia FuhrmannInstitut Curie, PSL Research University, Pathology-Genetics-Immunology Department, 26 rue d'Ulm, F-75005, Paris, France.
Sophie VacherDepartment of Genetics, Institut Curie, PSL Research University, Pharmacogenomic Unit, 26 rue d'Ulm, F-75005, Paris, France.
Sonia Agüera-GonzálezInstitut Curie, PSL Research University, CNRS UMR144, Membrane and Cytoskeleton Dynamics group, 26 rue d'Ulm, F-75005, Paris, France.
Anna Zagryazhskaya-MassonInstitut Curie, PSL Research University, CNRS UMR144, Membrane and Cytoskeleton Dynamics group, 26 rue d'Ulm, F-75005, Paris, France.
Maryse RomaoInstitut Curie, PSL Research University, CNRS UMR144, Biogenesis and Functions of Lysosome-Related Organelles group, 26 rue d'Ulm, F-75005, Paris, France.
Carole El KesrouaniInstitut Curie, PSL Research University, Pathology-Genetics-Immunology Department, 26 rue d'Ulm, F-75005, Paris, France.
Angelika A NoegelCenter for Biochemistry, Institute of Biochemistry I, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 52, 50931, Cologne, Germany.
Thierry DuboisInstitut Curie, PSL Research University, Translational Research Department, Breast Cancer Biology Group, Paris, France.
Graça RaposoInstitut Curie, PSL Research University, CNRS UMR144, Biogenesis and Functions of Lysosome-Related Organelles group, 26 rue d'Ulm, F-75005, Paris, France.
James E BearUNC Lineberger Comprehensive Cancer Center and the Department of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.
Christoph S ClemenCenter for Biochemistry, Institute of Biochemistry I, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 52, 50931, Cologne, Germany.
Anne Vincent-SalomonInstitut Curie, PSL Research University, Pathology-Genetics-Immunology Department, 26 rue d'Ulm, F-75005, Paris, France.
Ivan BiècheDepartment of Genetics, Institut Curie, PSL Research University, Pharmacogenomic Unit, 26 rue d'Ulm, F-75005, Paris, France.
Philippe ChavrierInstitut Curie, PSL Research University, CNRS UMR144, Membrane and Cytoskeleton Dynamics group, 26 rue d'Ulm, F-75005, Paris, France. philippe.chavrier@curie.fr.ORCID http://orcid.org/0000-0002-7351-733X
Centre National de la Recherche Scientifique · FRUniversité Paris Sciences et Lettres · FRUniversity of Cologne · DEDélégation Paris 5 · FRUniversity of North Carolina at Chapel Hill · US

Funding

Systematic Analysis of the Actin Cytoskeleton and Directed Cell MigrationR35GM130312 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JAMES E BEAR · 2019 to 2026
$4.8M
Agence Nationale de la Recherche (French National Research Agency) ANR-10-LBX-0038Deutsche Forschungsgemeinschaft (German Research Foundation) DFG NO 113/22-2European Molecular Biology Organization (EMBO) Long-Term postdoc fellowshipInstitut National Du Cancer (French National Cancer Institute) 6521NIGMS NIH HHS R35 GM130312Worldwide Cancer Research 16-1235
6 · The paper itself

Abstract

Membrane type 1-matrix metalloproteinase (MT1-MMP), a membrane-tethered protease, is key for matrix breakdown during cancer invasion and metastasis. Assembly of branched actin networks by the Arp2/3 complex is required for MT1-MMP traffic and formation of matrix-degradative invadopodia. Contrasting with the well-established role of actin filament branching factor cortactin in invadopodia function during cancer cell invasion, the contribution of coronin-family debranching factors to invadopodia-based matrix remodeling is not known. Here, we investigated the contribution of coronin 1C to the invasive potential of breast cancer cells. We report that expression of coronin 1C is elevated in invasive human breast cancers, correlates positively with MT1-MMP expression in relation with increased metastatic risk and is a new independent prognostic factor in breast cancer. We provide evidence that, akin to cortactin, coronin 1C is required for invadopodia formation and matrix degradation by breast cancer cells lines and for 3D collagen invasion by multicellular spheroids. Using intravital imaging of orthotopic human breast tumor xenografts, we find that coronin 1C accumulates in structures forming in association with collagen fibrils in the tumor microenvironment. Moreover, we establish the role of coronin 1C in the regulation of positioning and trafficking of MT1-MMP-positive endolysosomes. These results identify coronin 1C as a novel player of the multi-faceted mechanism responsible for invadopodia formation, MT1-MMP surface exposure and invasiveness in breast cancer cells.

Indexed as

AnimalsCell Line, TumorFemaleHeterograftsHumansMatrix Metalloproteinase 14MiceMicrofilament ProteinsNeoplasm InvasivenessPodosomesProtein TransportSpheroids, CellularTriple Negative Breast Neoplasmscoronin proteinsMatrix Metalloproteinase 14Microfilament ProteinsMMP14 protein, human

Identifiers

PMID30065298
OpenAlexW2886412256

What OpenQuestion holds

Textmetadata
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.