IRE1 endoribonuclease signaling promotes myeloid cell infiltration in glioblastoma.
Fiche publication
Date publication
décembre 2023
Journal
Neuro-oncology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr MARTIN Sophie, Dr NEGRONI Luc
Tous les auteurs :
Obacz J, Archambeau J, Lafont E, Nivet M, Martin S, Aubry M, Voutetakis K, Pineau R, Boniface R, Sicari D, Pelizzari-Raymundo D, Ghukasyan G, McGrath E, Vlachavas EI, Le Gallo M, Le Reste PJ, Barroso K, Fainsod-Levi T, Obiedat A, Granot Z, Tirosh B, Samal J, Pandit A, Négroni L, Soriano N, Monnier A, Mosser J, Chatziioannou A, Quillien V, Chevet E, Avril T
Lien Pubmed
Résumé
Intrinsic or environmental stresses trigger the accumulation of improperly folded proteins in the endoplasmic reticulum (ER), leading to ER stress. To cope with this, cells have evolved an adaptive mechanism named the unfolded protein response (UPR) which is hijacked by tumor cells to develop malignant features. Glioblastoma (GB), the most aggressive and lethal primary brain tumor, relies on UPR to sustain growth. We recently showed that IRE1 alpha (referred to IRE1 hereafter), one of the UPR transducers, promotes GB invasion, angiogenesis and infiltration by macrophage. Hence, high tumor IRE1 activity in tumor cells predicts worse outcome. Herein, we characterized the IRE1-dependent signaling that shapes the immune microenvironment towards monocytes/macrophages and neutrophils.
Mots clés
ER stress, IRE1, chemokines, glioblastoma, inflammation
Référence
Neuro Oncol. 2023 12 28;: