SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer

SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer

The capacity of cancer cells to migrate is intimately linked to their ability to induce metastasis. Here the authors show that the sodium channel β4 subunit regulates breast cancer cell migration via inhibition of RhoA activation, independently from its function as an auxiliary protein of the sodium...

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Main Authors: Emeline Bon, Virginie Driffort, Frédéric Gradek, Carlos Martinez-Caceres, Monique Anchelin, Pablo Pelegrin, Maria-Luisa Cayuela, Séverine Marionneau-Lambot, Thibauld Oullier, Roseline Guibon, Gaëlle Fromont, Jorge L. Gutierrez-Pajares, Isabelle Domingo, Eric Piver, Alain Moreau, Julien Burlaud-Gaillard, Philippe G. Frank, Stéphan Chevalier, Pierre Besson, Sébastien Roger
Format: Article
Language:English
Published: Nature Publishing Group 2016-12-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms13648
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spelling doaj-b868edb8e4164085a3574d6fbc6f262e2021-05-11T11:11:47ZengNature Publishing GroupNature Communications2041-17232016-12-017111810.1038/ncomms13648SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancerEmeline Bon0Virginie Driffort1Frédéric Gradek2Carlos Martinez-Caceres3Monique Anchelin4Pablo Pelegrin5Maria-Luisa Cayuela6Séverine Marionneau-Lambot7Thibauld Oullier8Roseline Guibon9Gaëlle Fromont10Jorge L. Gutierrez-Pajares11Isabelle Domingo12Eric Piver13Alain Moreau14Julien Burlaud-Gaillard15Philippe G. Frank16Stéphan Chevalier17Pierre Besson18Sébastien Roger19Inserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursInflammation and Experimental Surgery Unit, CIBERehd, Murcia’s BioHealth Research Institute IMIB-Arrixaca, Clinical University Hospital Virgen de la ArrixacaTelomerase, Cancer and Aging Group, Hospital Virgen de la ArrixacaInflammation and Experimental Surgery Unit, CIBERehd, Murcia’s BioHealth Research Institute IMIB-Arrixaca, Clinical University Hospital Virgen de la ArrixacaTelomerase, Cancer and Aging Group, Hospital Virgen de la ArrixacaCancéropôle du Grand Ouest, Plateforme In VivoCancéropôle du Grand Ouest, Plateforme In VivoInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursCHRU de Tours, 2 Boulevard TonnelléInserm, U966, Université François-Rabelais de ToursLaboratoire de Biologie Cellulaire-Microscopie Electronique, Faculté de Médecine, Université François-Rabelais de ToursInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursInserm UMR1069, Nutrition, Croissance et Cancer, Université François-Rabelais de ToursThe capacity of cancer cells to migrate is intimately linked to their ability to induce metastasis. Here the authors show that the sodium channel β4 subunit regulates breast cancer cell migration via inhibition of RhoA activation, independently from its function as an auxiliary protein of the sodium channel.https://doi.org/10.1038/ncomms13648
collection DOAJ
language English
format Article
sources DOAJ
author Emeline Bon
Virginie Driffort
Frédéric Gradek
Carlos Martinez-Caceres
Monique Anchelin
Pablo Pelegrin
Maria-Luisa Cayuela
Séverine Marionneau-Lambot
Thibauld Oullier
Roseline Guibon
Gaëlle Fromont
Jorge L. Gutierrez-Pajares
Isabelle Domingo
Eric Piver
Alain Moreau
Julien Burlaud-Gaillard
Philippe G. Frank
Stéphan Chevalier
Pierre Besson
Sébastien Roger
spellingShingle Emeline Bon
Virginie Driffort
Frédéric Gradek
Carlos Martinez-Caceres
Monique Anchelin
Pablo Pelegrin
Maria-Luisa Cayuela
Séverine Marionneau-Lambot
Thibauld Oullier
Roseline Guibon
Gaëlle Fromont
Jorge L. Gutierrez-Pajares
Isabelle Domingo
Eric Piver
Alain Moreau
Julien Burlaud-Gaillard
Philippe G. Frank
Stéphan Chevalier
Pierre Besson
Sébastien Roger
SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer
Nature Communications
author_facet Emeline Bon
Virginie Driffort
Frédéric Gradek
Carlos Martinez-Caceres
Monique Anchelin
Pablo Pelegrin
Maria-Luisa Cayuela
Séverine Marionneau-Lambot
Thibauld Oullier
Roseline Guibon
Gaëlle Fromont
Jorge L. Gutierrez-Pajares
Isabelle Domingo
Eric Piver
Alain Moreau
Julien Burlaud-Gaillard
Philippe G. Frank
Stéphan Chevalier
Pierre Besson
Sébastien Roger
author_sort Emeline Bon
title SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer
title_short SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer
title_full SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer
title_fullStr SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer
title_full_unstemmed SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer
title_sort scn4b acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2016-12-01
description The capacity of cancer cells to migrate is intimately linked to their ability to induce metastasis. Here the authors show that the sodium channel β4 subunit regulates breast cancer cell migration via inhibition of RhoA activation, independently from its function as an auxiliary protein of the sodium channel.
url https://doi.org/10.1038/ncomms13648
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