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The Autophagy Machinery: A New Player in Chemotactic Cell Migration

Autophagy is a highly conserved self-degradative process that plays a key role in diverse cellular processes such as stress response or differentiation. A growing body of work highlights the direct involvement of autophagy in cell migration and cancer metastasis. Specifically, autophagy has been sho...

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Autores principales: Coly, Pierre-Michaël, Gandolfo, Pierrick, Castel, Hélène, Morin, Fabrice
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5311050/
https://www.ncbi.nlm.nih.gov/pubmed/28261054
http://dx.doi.org/10.3389/fnins.2017.00078
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author Coly, Pierre-Michaël
Gandolfo, Pierrick
Castel, Hélène
Morin, Fabrice
author_facet Coly, Pierre-Michaël
Gandolfo, Pierrick
Castel, Hélène
Morin, Fabrice
author_sort Coly, Pierre-Michaël
collection PubMed
description Autophagy is a highly conserved self-degradative process that plays a key role in diverse cellular processes such as stress response or differentiation. A growing body of work highlights the direct involvement of autophagy in cell migration and cancer metastasis. Specifically, autophagy has been shown to be involved in modulating cell adhesion dynamics as well as epithelial-to-mesenchymal transition. After providing a general overview of the mechanisms controlling autophagosome biogenesis and cell migration, we discuss how chemotactic G protein-coupled receptors, through the repression of autophagy, may orchestrate membrane trafficking and compartmentation of specific proteins at the cell front in order to support the critical steps of directional migration.
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spelling pubmed-53110502017-03-03 The Autophagy Machinery: A New Player in Chemotactic Cell Migration Coly, Pierre-Michaël Gandolfo, Pierrick Castel, Hélène Morin, Fabrice Front Neurosci Endocrinology Autophagy is a highly conserved self-degradative process that plays a key role in diverse cellular processes such as stress response or differentiation. A growing body of work highlights the direct involvement of autophagy in cell migration and cancer metastasis. Specifically, autophagy has been shown to be involved in modulating cell adhesion dynamics as well as epithelial-to-mesenchymal transition. After providing a general overview of the mechanisms controlling autophagosome biogenesis and cell migration, we discuss how chemotactic G protein-coupled receptors, through the repression of autophagy, may orchestrate membrane trafficking and compartmentation of specific proteins at the cell front in order to support the critical steps of directional migration. Frontiers Media S.A. 2017-02-16 /pmc/articles/PMC5311050/ /pubmed/28261054 http://dx.doi.org/10.3389/fnins.2017.00078 Text en Copyright © 2017 Coly, Gandolfo, Castel and Morin. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Coly, Pierre-Michaël
Gandolfo, Pierrick
Castel, Hélène
Morin, Fabrice
The Autophagy Machinery: A New Player in Chemotactic Cell Migration
title The Autophagy Machinery: A New Player in Chemotactic Cell Migration
title_full The Autophagy Machinery: A New Player in Chemotactic Cell Migration
title_fullStr The Autophagy Machinery: A New Player in Chemotactic Cell Migration
title_full_unstemmed The Autophagy Machinery: A New Player in Chemotactic Cell Migration
title_short The Autophagy Machinery: A New Player in Chemotactic Cell Migration
title_sort autophagy machinery: a new player in chemotactic cell migration
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5311050/
https://www.ncbi.nlm.nih.gov/pubmed/28261054
http://dx.doi.org/10.3389/fnins.2017.00078
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