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

Autores
Castagnino, Alessia; Castro Castro, Antonio; Irondelle, Marie; Guichard, Alan; Lodillinsky, Catalina; Fuhrmann, Laetitia; Vacher, Sophie; Agüera González, Sonia; Zagryazhskaya Masson, Anna; Romao, Maryse; El Kesrouani, Carole; Noegel, Angelika A.; Dubois, Thierry; Raposo, Graça; Bear, James E.; Clemen, Christoph S.; Vincent Salomon, Anne; Bièche, Ivan; Chavrier, Philippe
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
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.
Fil: Castagnino, Alessia. Institute Curie; Francia
Fil: Castro Castro, Antonio. Institute Curie; Francia
Fil: Irondelle, Marie. Institute Curie; Francia
Fil: Guichard, Alan. Institute Curie; Francia
Fil: Lodillinsky, Catalina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Fuhrmann, Laetitia. Institute Curie; Francia
Fil: Vacher, Sophie. Institute Curie; Francia
Fil: Agüera González, Sonia. Institute Curie; Francia
Fil: Zagryazhskaya Masson, Anna. Institute Curie; Francia
Fil: Romao, Maryse. Institute Curie; Francia
Fil: El Kesrouani, Carole. Institute Curie; Francia
Fil: Noegel, Angelika A.. Institute Curie; Francia
Fil: Dubois, Thierry. Institute Curie; Francia
Fil: Raposo, Graça. Institute Curie; Francia
Fil: Bear, James E.. Institute Curie; Francia
Fil: Clemen, Christoph S.. Institute Curie; Francia
Fil: Vincent Salomon, Anne. Institute Curie; Francia
Fil: Bièche, Ivan. Institute Curie; Francia
Fil: Chavrier, Philippe. Institute Curie; Francia
Materia
CORONIN
MT1-MMP
BREAST CANCER
CELL INVASION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/153104
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/153104
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia functionCastagnino, AlessiaCastro Castro, AntonioIrondelle, MarieGuichard, AlanLodillinsky, CatalinaFuhrmann, LaetitiaVacher, SophieAgüera González, SoniaZagryazhskaya Masson, AnnaRomao, MaryseEl Kesrouani, CaroleNoegel, Angelika A.Dubois, ThierryRaposo, GraçaBear, James E.Clemen, Christoph S.Vincent Salomon, AnneBièche, IvanChavrier, PhilippeCORONINMT1-MMPBREAST CANCERCELL INVASIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Membrane 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.Fil: Castagnino, Alessia. Institute Curie; FranciaFil: Castro Castro, Antonio. Institute Curie; FranciaFil: Irondelle, Marie. Institute Curie; FranciaFil: Guichard, Alan. Institute Curie; FranciaFil: Lodillinsky, Catalina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Fuhrmann, Laetitia. Institute Curie; FranciaFil: Vacher, Sophie. Institute Curie; FranciaFil: Agüera González, Sonia. Institute Curie; FranciaFil: Zagryazhskaya Masson, Anna. Institute Curie; FranciaFil: Romao, Maryse. Institute Curie; FranciaFil: El Kesrouani, Carole. Institute Curie; FranciaFil: Noegel, Angelika A.. Institute Curie; FranciaFil: Dubois, Thierry. Institute Curie; FranciaFil: Raposo, Graça. Institute Curie; FranciaFil: Bear, James E.. Institute Curie; FranciaFil: Clemen, Christoph S.. Institute Curie; FranciaFil: Vincent Salomon, Anne. Institute Curie; FranciaFil: Bièche, Ivan. Institute Curie; FranciaFil: Chavrier, Philippe. Institute Curie; FranciaNature Publishing Group2018-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/153104Castagnino, Alessia; Castro Castro, Antonio; Irondelle, Marie; Guichard, Alan; Lodillinsky, Catalina; et al.; Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function; Nature Publishing Group; Oncogene; 7-2018; 1-170950-9232CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.nature.com/articles/s41388-018-0422-xinfo:eu-repo/semantics/altIdentifier/doi/10.1038/s41388-018-0422-xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:39:53Zoai:ri.conicet.gov.ar:11336/153104instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:39:53.447CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function
title Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function
spellingShingle Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function
Castagnino, Alessia
CORONIN
MT1-MMP
BREAST CANCER
CELL INVASION
title_short Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function
title_full Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function
title_fullStr Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function
title_full_unstemmed Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function
title_sort Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function
dc.creator.none.fl_str_mv Castagnino, Alessia
Castro Castro, Antonio
Irondelle, Marie
Guichard, Alan
Lodillinsky, Catalina
Fuhrmann, Laetitia
Vacher, Sophie
Agüera González, Sonia
Zagryazhskaya Masson, Anna
Romao, Maryse
El Kesrouani, Carole
Noegel, Angelika A.
Dubois, Thierry
Raposo, Graça
Bear, James E.
Clemen, Christoph S.
Vincent Salomon, Anne
Bièche, Ivan
Chavrier, Philippe
author Castagnino, Alessia
author_facet Castagnino, Alessia
Castro Castro, Antonio
Irondelle, Marie
Guichard, Alan
Lodillinsky, Catalina
Fuhrmann, Laetitia
Vacher, Sophie
Agüera González, Sonia
Zagryazhskaya Masson, Anna
Romao, Maryse
El Kesrouani, Carole
Noegel, Angelika A.
Dubois, Thierry
Raposo, Graça
Bear, James E.
Clemen, Christoph S.
Vincent Salomon, Anne
Bièche, Ivan
Chavrier, Philippe
author_role author
author2 Castro Castro, Antonio
Irondelle, Marie
Guichard, Alan
Lodillinsky, Catalina
Fuhrmann, Laetitia
Vacher, Sophie
Agüera González, Sonia
Zagryazhskaya Masson, Anna
Romao, Maryse
El Kesrouani, Carole
Noegel, Angelika A.
Dubois, Thierry
Raposo, Graça
Bear, James E.
Clemen, Christoph S.
Vincent Salomon, Anne
Bièche, Ivan
Chavrier, Philippe
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv CORONIN
MT1-MMP
BREAST CANCER
CELL INVASION
topic CORONIN
MT1-MMP
BREAST CANCER
CELL INVASION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv 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.
Fil: Castagnino, Alessia. Institute Curie; Francia
Fil: Castro Castro, Antonio. Institute Curie; Francia
Fil: Irondelle, Marie. Institute Curie; Francia
Fil: Guichard, Alan. Institute Curie; Francia
Fil: Lodillinsky, Catalina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Fuhrmann, Laetitia. Institute Curie; Francia
Fil: Vacher, Sophie. Institute Curie; Francia
Fil: Agüera González, Sonia. Institute Curie; Francia
Fil: Zagryazhskaya Masson, Anna. Institute Curie; Francia
Fil: Romao, Maryse. Institute Curie; Francia
Fil: El Kesrouani, Carole. Institute Curie; Francia
Fil: Noegel, Angelika A.. Institute Curie; Francia
Fil: Dubois, Thierry. Institute Curie; Francia
Fil: Raposo, Graça. Institute Curie; Francia
Fil: Bear, James E.. Institute Curie; Francia
Fil: Clemen, Christoph S.. Institute Curie; Francia
Fil: Vincent Salomon, Anne. Institute Curie; Francia
Fil: Bièche, Ivan. Institute Curie; Francia
Fil: Chavrier, Philippe. Institute Curie; Francia
description 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.
publishDate 2018
dc.date.none.fl_str_mv 2018-07
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/153104
Castagnino, Alessia; Castro Castro, Antonio; Irondelle, Marie; Guichard, Alan; Lodillinsky, Catalina; et al.; Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function; Nature Publishing Group; Oncogene; 7-2018; 1-17
0950-9232
CONICET Digital
CONICET
url http://hdl.handle.net/11336/153104
identifier_str_mv Castagnino, Alessia; Castro Castro, Antonio; Irondelle, Marie; Guichard, Alan; Lodillinsky, Catalina; et al.; Coronin 1C promotes triple-negative breast cancer invasiveness through regulation of MT1-MMP traffic and invadopodia function; Nature Publishing Group; Oncogene; 7-2018; 1-17
0950-9232
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.nature.com/articles/s41388-018-0422-x
info:eu-repo/semantics/altIdentifier/doi/10.1038/s41388-018-0422-x
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Nature Publishing Group
publisher.none.fl_str_mv Nature Publishing Group
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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