2023•Unpublished venueOpen access
Supplemental Figure S7 from CRMP5 Controls Glioblastoma Cell Proliferation and Survival through Notch-Dependent Signaling
Aubin Moutal, Jérôme Honnorat, Patrick Massoma, Pauline Désormeaux, Caroline Bertrand, Céline Malleval, Chantal Watrin, Naura Chounlamountri, Marie-Eve Mayeur, Roger Besançon, Nicolas Naudet, Léa Magadoux, Rajesh Khanna, François Ducray, David Meyronet, Nicole Thomasset
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Abstract
Working model of CRMP5 mechanism to control Notch signaling pathway and cellular proliferation in GBM. (1) Notch receptors are expressed in GBM and activated by interaction with their ligands (2) After activation, notch is cleaved by the γ-secretase complex and (3) the Notch intracellular domain (NICD) is translocated in the nucleus. (4) activates its target genes (hes1, hey1) promoting tumor cells proliferation. Notch activates, by an unknown mechanism, Akt which is another event increasing GBM proliferation and survival and leading to poor patient survival. (6) Notch signaling pathway inhibition is mediated by the E3 ubiquitin ligase (Itch) recruitment which (7) targets the Notch receptors into lysosomal degradation, resulting in Notch signaling pathway inhibition. These events are correlated with increased survival of patients. (8) CRMP5 is expressed in GBM and promotes the Notch signaling pathway over Itch-induced degradation of the Notch receptors thereby leading to sustained activation of the Notch signaling pathway, increased proliferation resulting in decreased overall survival of patients