Titre :

Homeostasis and Autophagy Enhances Cancer Cells'' Chemosensitivity.

Auteur(s) :

Dubois, Charlotte [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Physiologie Cellulaire (PHYCELL) - U1003
Kondratskyi, A. [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Bidaux, Gabriel [Auteur]
Cardiovasculaire, métabolisme, diabétologie et nutrition [CarMeN]
Noyer, Lucile [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Vancauwenberghe, E. [Auteur]
Farfariello, Valerio [Auteur]
Physiologie Cellulaire (PHYCELL) - U1003
Toillon, Robert [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies (CANTHER) - UMR 9020 - UMR 1277
Roudbaraki, Morad [Auteur]
Physiologie Cellulaire (PHYCELL) - U1003
Tierny, Dominique [Auteur]
Oncovet
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Bonnal, Jean-Louis [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Physiologie Cellulaire (PHYCELL) - U1003
Prevarskaya, Natalia [Auteur]
Physiologie Cellulaire (PHYCELL) - U1003
Vanden Abeele, Fabien [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Physiologie Cellulaire (PHYCELL) - U1003

Titre de la revue :

iScience

Nom court de la revue :

Iscience

Numéro :

23

Pagination :

101263

Date de publication :

2020-06-27

ISSN :

2589-0042

Discipline(s) HAL :

Sciences du Vivant [q-bio]

Résumé en anglais : [en]

Mitochondria are important cell death checkpoints, and mitochondrial Ca2+ overload is considered as a potent apoptotic intrinsic pathway inducer. Here, we report that this Ca2+ apoptosis link is largely ineffective in ...
Lire la suite >Mitochondria are important cell death checkpoints, and mitochondrial Ca2+ overload is considered as a potent apoptotic intrinsic pathway inducer. Here, we report that this Ca2+ apoptosis link is largely ineffective in inducing cell-death just by itself and required a concomitant inhibition of autophagy to counteract its pro-survival action. In such condition, an acute mitochondrial stress revealed by a DRP1-mediated mitochondrial dynamic remodeling is observed concomitantly with mitochondrial depolarization, release of cytochrome c, and efficient apoptosis induction. We also uncover that mitochondrial Ca2+ status modulates the function of autophagy as a sensitizer for chemotherapies. This priming mediated by mitochondrial Ca2+ overload and inhibition of autophagy sensitizes many cancer cells types to different chemotherapies with independent mechanisms of action. Collectively, our results redefine an important cell signaling pathway, uncovering new combined therapies for the treatment of diseases associated with mitochondrial Ca2+ homeostasis disorders such as cancer.Lire moins >

Comité de lecture :

Oui

Audience :

Internationale

Vulgarisation :

Non

Établissement(s) :

Université de Lille
Inserm
CHU Lille

Collections :

• Cancer Heterogeneity, Plasticity and Resistance to Therapies (CANTHER) - UMR 9020 - UMR 1277
• Physiologie Cellulaire (PHYCELL) - U1003
• Plasticité Cellulaire et Cancer (CPAC) - U908
• Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192

Date de dépôt :

2023-12-13T05:22:32Z
2024-01-31T11:05:42Z