ORAI3 silencing alters cell proliferation ...
Document type :
Article dans une revue scientifique: Article original
PMID :
Title :
ORAI3 silencing alters cell proliferation and promotes mitotic catastrophe and apoptosis in pancreatic adenocarcinoma.
Author(s) :
Ziental Gelus, Nathalie [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Vanden Abeele, Fabien [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Dubois, Charlotte [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Kondratska, Kateryna [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Kondratskyi, Artem [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Morabito, Angela [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Mesilmany, Lina [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Farfariello, Valerio [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Toillon, Robert [Auteur]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Gelus, Nathalie [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Laurenge, Emilie [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Lemonnier, Loic [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Prevarskaya, Natalia [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Vanden Abeele, Fabien [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Dubois, Charlotte [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Kondratska, Kateryna [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Kondratskyi, Artem [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Morabito, Angela [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Mesilmany, Lina [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Farfariello, Valerio [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Toillon, Robert [Auteur]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Gelus, Nathalie [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Laurenge, Emilie [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Lemonnier, Loic [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Prevarskaya, Natalia [Auteur]
Laboratoire de Physiologie Cellulaire - U 1003 [PHYCELL]
Journal title :
Biochimica et Biophysica Acta - Molecular Cell Research
Pages :
119023
Publisher :
Elsevier
Publication date :
2021-03
ISSN :
0167-4889
English keyword(s) :
Apoptosis
Calcium channels
Mitotic catastrophe
ORAI3
PDAC
Calcium channels
Mitotic catastrophe
ORAI3
PDAC
HAL domain(s) :
Sciences du Vivant [q-bio]/Biologie cellulaire
English abstract : [en]
Changes in cytosolic free Ca2+ concentration play a central role in many fundamental cellular processes including muscle contraction, neurotransmission, cell proliferation, differentiation, gene transcription and cell ...
Show more >Changes in cytosolic free Ca2+ concentration play a central role in many fundamental cellular processes including muscle contraction, neurotransmission, cell proliferation, differentiation, gene transcription and cell death. Many of these processes are known to be regulated by store-operated calcium channels (SOCs), among which ORAI1 is the most studied in cancer cells, leaving the role of other ORAI channels yet inadequately addressed. Here we demonstrate that ORAI3 channels are expressed in both normal (HPDE) and pancreatic ductal adenocarcinoma (PDAC) cell lines, where they form functional channels, their knockdown affecting store operated calcium entry (SOCE). More specifically, ORAI3 silencing increased SOCE in PDAC cell lines, while decreasing SOCE in normal pancreatic cell line. We also show the role of ORAI3 in proliferation, cell cycle, viability, mitotic catastrophe and cell death. Finally, we demonstrate that ORAI3 silencing impairs pancreatic tumor growth and induces cell death in vivo, suggesting that ORAI3 could represent a potential therapeutic target in PDAC treatment.Show less >
Show more >Changes in cytosolic free Ca2+ concentration play a central role in many fundamental cellular processes including muscle contraction, neurotransmission, cell proliferation, differentiation, gene transcription and cell death. Many of these processes are known to be regulated by store-operated calcium channels (SOCs), among which ORAI1 is the most studied in cancer cells, leaving the role of other ORAI channels yet inadequately addressed. Here we demonstrate that ORAI3 channels are expressed in both normal (HPDE) and pancreatic ductal adenocarcinoma (PDAC) cell lines, where they form functional channels, their knockdown affecting store operated calcium entry (SOCE). More specifically, ORAI3 silencing increased SOCE in PDAC cell lines, while decreasing SOCE in normal pancreatic cell line. We also show the role of ORAI3 in proliferation, cell cycle, viability, mitotic catastrophe and cell death. Finally, we demonstrate that ORAI3 silencing impairs pancreatic tumor growth and induces cell death in vivo, suggesting that ORAI3 could represent a potential therapeutic target in PDAC treatment.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Collections :
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