Academic Journal
p65/RelA NF‐κB fragments generated by RIPK3 activity regulate tumorigenicity, cell metabolism, and stemness characteristics
| العنوان: | p65/RelA NF‐κB fragments generated by RIPK3 activity regulate tumorigenicity, cell metabolism, and stemness characteristics |
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| المؤلفون: | Touil, Yasmine, Latreche‐carton, Céline, Bouazzati, Hassiba El, Nugues, Anne‐lucie, Jouy, Nathalie, Thuru, Xavier, Laine, William, Lepretre, Frederic, Figeac, Martin, Tardivel, Meryem, Kluza, Jérôme, Idziorek, Thierry, Quesnel, Bruno |
| المساهمون: | Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Pasteur Network (Réseau International des Instituts Pasteur)-Pasteur Network (Réseau International des Instituts Pasteur)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire CHU Lille (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Institut pour la recherche sur le cancer de Lille Lille (IRCL), Plateforme BioImaging Center Lille - PLBS (BICeL), Plateformes Lilloises en Biologie et Santé - UAR 2014 - US 41 (PLBS), Pasteur Network (Réseau International des Instituts Pasteur)-Pasteur Network (Réseau International des Instituts Pasteur)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire CHU Lille (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur de Lille, Service des Maladies du Sang CHU Lille (SMS), Hôpital Claude Huriez Lille, Centre Hospitalier Régional Universitaire CHU Lille (CHRU Lille)-Centre Hospitalier Régional Universitaire CHU Lille (CHRU Lille) |
| المصدر: | ISSN: 0730-2312. |
| بيانات النشر: | CCSD Wiley |
| سنة النشر: | 2022 |
| المجموعة: | LillOA (HAL Lille Open Archive, Université de Lille) |
| مصطلحات موضوعية: | RIPK3, cancer, fragment, p65/RelA, stemness, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC] |
| الوصف: | International audience ; 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. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| Relation: | info:eu-repo/semantics/altIdentifier/pmid/34927768; PUBMED: 34927768; PUBMEDCENTRAL: PMC9299825 |
| DOI: | 10.1002/jcb.30198 |
| الاتاحة: | https://hal.science/hal-03641788 https://hal.science/hal-03641788v1/document https://hal.science/hal-03641788v1/file/J%20of%20Cellular%20Biochemistry%20-%202021%20-%20Touil.pdf https://doi.org/10.1002/jcb.30198 |
| Rights: | info:eu-repo/semantics/OpenAccess |
| رقم الانضمام: | edsbas.C648840B |
| قاعدة البيانات: | BASE |
| DOI: | 10.1002/jcb.30198 |
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