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p65/RelA NF‐κB fragments generated by RIPK3 ...
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Document type :
Article dans une revue scientifique: Article original
DOI :
10.1002/jcb.30198
PMID :
34927768
Title :
p65/RelA NF‐κB fragments generated by RIPK3 activity regulate tumorigenicity, cell metabolism, and stemness characteristics
Author(s) :
Touil, Yasmine [Auteur]
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Latreche‐carton, Céline [Auteur]
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Bouazzati, Hassiba El [Auteur]
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Nugues, Anne‐lucie [Auteur]
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Jouy, Nathalie [Auteur]
Plateforme BioImaging Center Lille - PLBS [BICeL]
Thuru, Xavier [Auteur] refId
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Laine, William [Auteur]
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Lepretre, Frederic [Auteur]
Plateforme BioImaging Center Lille - PLBS [BICeL]
Figeac, Martin [Auteur] refId
Plateforme BioImaging Center Lille - PLBS [BICeL]
Tardivel, Meryem [Auteur] refId
Plateformes Lilloises en Biologie et Santé - UAR 2014 - US 41 [PLBS]
Kluza, Jerome [Auteur] refId
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Idziorek, Thierry [Auteur] refId
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Quesnel, Bruno [Auteur]
Service des Maladies du Sang [CHU Lille] [SMS]
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Journal title :
Journal of Cellular Biochemistry
Pages :
543-556
Publisher :
Wiley
Publication date :
2022
ISSN :
0730-2312
English keyword(s) :
RIPK3
cancer
fragment
p65/RelA
stemness.
HAL domain(s) :
Sciences du Vivant [q-bio]/Cancer
Sciences du Vivant [q-bio]/Biochimie, Biologie Moléculaire
Sciences du Vivant [q-bio]/Biologie cellulaire/Organisation et fonctions cellulaires [q-bio.SC]
English abstract : [en]
Receptor-interacting protein kinase 3 (RIPK3) can induce necroptosis, apoptosis, or cell proliferation and is silenced in several hematological malignancies. We previously reported that RIPK3 activity independent of its ...
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Receptor-interacting protein kinase 3 (RIPK3) can induce necroptosis, apoptosis, or cell proliferation and is silenced in several hematological malignancies. We previously reported that RIPK3 activity independent of its kinase domain induces caspase-mediated p65/RelA cleavage, resulting in N-terminal 1-361 and C-terminal 362-549 fragments. We show here that a noncleavable p65/RelA D361E mutant expressed in DA1-3b leukemia cells decreases mouse survival times and that coexpression of p65/RelA fragments increases the tumorigenicity of B16F1 melanoma cells. This aggressiveness in vivo did not correlate with NF-κB activity measured in vitro. The fragments and p65/RelA D361E mutant induced different expression profiles in DA1-3b and B16F1 cells. Stemness markers were affected: p65/RelA D361E increased ALDH activity in DA1-3b cells, and fragment expression increased melanoma sphere formation in B16/F1 cells. p65/RelA fragments and the D361E noncleavable mutant decreased oxidative or glycolytic cell metabolism, with differences observed between models. Thus, p65/RelA cleavage initiated by kinase-independent RIPK3 activity in cancer cells is not neutral and induces pleiotropic effects in vitro and in vivo that may vary across tumor types.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Collections :
  • Cancer Heterogeneity, Plasticity and Resistance to Therapies (CANTHER) - UMR 9020 - UMR 1277
Source :
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