Galectin-3 modulates epithelial cell ...
Title :
Galectin-3 modulates epithelial cell adaptation to stress at the ER-mitochondria interface
Author(s) :
Coppin, Lucie [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Jannin, Arnaud [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Ait Yahya, Emilie [Auteur]
Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille]
Thuillier, Caroline [Auteur]
Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille]
Villenet, Céline [Auteur]
Plateforme de génomique fonctionnelle et structurelle [Lille]
Tardivel, Meryem [Auteur]
Bongiovanni, Antonino [Auteur]
Gaston, Cécile [Auteur]
Institut Jacques Monod [IJM (UMR_7592)]
de Beco, Simon [Auteur]
Institut Jacques Monod [IJM (UMR_7592)]
Barois, Nicolas [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
VAN SEUNINGEN, ISABELLE [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Durand, Emmanuelle [Auteur]
Metabolic functional (epi)genomics and molecular mechanisms involved in type 2 diabetes and related diseases - UMR 8199 - UMR 1283 [EGENODIA (GI3M)]
Bonnefond, Amélie [Auteur]
Metabolic functional (epi)genomics and molecular mechanisms involved in type 2 diabetes and related diseases - UMR 8199 - UMR 1283 [EGENODIA (GI3M)]
Vienne, Jean-Claude [Auteur]
Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille]
Vamecq, Joseph [Auteur]
Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille]
Figeac, Martin [Auteur]
Plateforme de génomique fonctionnelle et structurelle [Lille]
Vincent, Audrey [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Delacour, Delphine [Auteur]
Institut Jacques Monod [IJM (UMR_7592)]
Porchet, Nicole [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Pigny, Pascal [Auteur correspondant]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]

Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Jannin, Arnaud [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Ait Yahya, Emilie [Auteur]
Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille]
Thuillier, Caroline [Auteur]
Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille]
Villenet, Céline [Auteur]
Plateforme de génomique fonctionnelle et structurelle [Lille]
Tardivel, Meryem [Auteur]
Bongiovanni, Antonino [Auteur]
Gaston, Cécile [Auteur]
Institut Jacques Monod [IJM (UMR_7592)]
de Beco, Simon [Auteur]
Institut Jacques Monod [IJM (UMR_7592)]
Barois, Nicolas [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
VAN SEUNINGEN, ISABELLE [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Durand, Emmanuelle [Auteur]
Metabolic functional (epi)genomics and molecular mechanisms involved in type 2 diabetes and related diseases - UMR 8199 - UMR 1283 [EGENODIA (GI3M)]
Bonnefond, Amélie [Auteur]
Metabolic functional (epi)genomics and molecular mechanisms involved in type 2 diabetes and related diseases - UMR 8199 - UMR 1283 [EGENODIA (GI3M)]
Vienne, Jean-Claude [Auteur]
Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille]
Vamecq, Joseph [Auteur]
Centre Hospitalier Régional Universitaire [Lille] [CHRU Lille]
Figeac, Martin [Auteur]
Plateforme de génomique fonctionnelle et structurelle [Lille]
Vincent, Audrey [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Delacour, Delphine [Auteur]
Institut Jacques Monod [IJM (UMR_7592)]
Porchet, Nicole [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Pigny, Pascal [Auteur correspondant]

Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Journal title :
Cell Death and Disease
Pages :
360
Publisher :
Nature Publishing Group
Publication date :
2020-05-12
ISSN :
2041-4889
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
Cellular stress response contributes to epithelial defense in adaptation to environment changes. Galectins play a pivotal role in the regulation of this response in malignant cells. However, precise underlying mechanisms ...
Show more >Cellular stress response contributes to epithelial defense in adaptation to environment changes. Galectins play a pivotal role in the regulation of this response in malignant cells. However, precise underlying mechanisms are largely unknown. Here we demonstrate that Galectin-3, a pro and anti-apoptotic lectin, is required for setting up a correct cellular response to stress by orchestrating several effects. First, Galectin-3 constitutes a key post-transcriptional regulator of stress-related mRNA regulons coordinating the cell metabolism, the mTORC1 complex or the unfolded protein response (UPR). Moreover, we demonstrated the presence of Galectin-3 with mitochondria-associated membranes (MAM), and its interaction with proteins located at the ER or mitochondrial membranes. There Galectin-3 prevents the activation and recruitment at the mitochondria of the regulator of mitochondria fission DRP-1. Accordingly, loss of Galectin-3 impairs mitochondrial morphology, with more fragmented and round mitochondria, and dynamics both in normal and cancer epithelial cells in basal conditions. Importantly, Galectin-3 deficient cells also display changes of the activity of the mitochondrial respiratory chain complexes, of the mTORC1/S6RP/4EBP1 translation pathway and reactive oxygen species levels. Regarding the ER, Galectin-3 did not modify the activities of the 3 branches of the UPR in basal conditions. However, Galectin-3 favours an adaptative UPR following ER stress induction by Thapsigargin treatment. Altogether, at the ER-mitochondria interface, Galectin-3 coordinates the functioning of the ER and mitochondria, preserves the integrity of mitochondrial network and modulates the ER stress response.Show less >
Show more >Cellular stress response contributes to epithelial defense in adaptation to environment changes. Galectins play a pivotal role in the regulation of this response in malignant cells. However, precise underlying mechanisms are largely unknown. Here we demonstrate that Galectin-3, a pro and anti-apoptotic lectin, is required for setting up a correct cellular response to stress by orchestrating several effects. First, Galectin-3 constitutes a key post-transcriptional regulator of stress-related mRNA regulons coordinating the cell metabolism, the mTORC1 complex or the unfolded protein response (UPR). Moreover, we demonstrated the presence of Galectin-3 with mitochondria-associated membranes (MAM), and its interaction with proteins located at the ER or mitochondrial membranes. There Galectin-3 prevents the activation and recruitment at the mitochondria of the regulator of mitochondria fission DRP-1. Accordingly, loss of Galectin-3 impairs mitochondrial morphology, with more fragmented and round mitochondria, and dynamics both in normal and cancer epithelial cells in basal conditions. Importantly, Galectin-3 deficient cells also display changes of the activity of the mitochondrial respiratory chain complexes, of the mTORC1/S6RP/4EBP1 translation pathway and reactive oxygen species levels. Regarding the ER, Galectin-3 did not modify the activities of the 3 branches of the UPR in basal conditions. However, Galectin-3 favours an adaptative UPR following ER stress induction by Thapsigargin treatment. Altogether, at the ER-mitochondria interface, Galectin-3 coordinates the functioning of the ER and mitochondria, preserves the integrity of mitochondrial network and modulates the ER stress response.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
ANR Project :
Collections :
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