Fiche publication
Date publication
novembre 2013
Auteurs
Membres identifiés du Cancéropôle Est :
Pr DECONINCK Eric
,
Pr GARNACHE-OTTOU Francine
Tous les auteurs :
Mollet L, Robinet P, Dubois M, Aurouet A, Normand T, Charpentier S, Sureau A, Grandclement C, Garnache-Ottou F, Deconinck E, Brule F, Rohrlich PS, Legrand A
Lien Pubmed
Résumé
GALIG gene expression induces apoptosis in cultured cells through a pathway still under investigation. It is highly expressed in leukocytes but weakly detectable in bone marrow, suggesting a role in the myeloid lineage homeostasis. We show here that GALIG-induced cell death is counteracted by the overexpression of MCL-1, a pro-survival member of the Bcl2 family. Moreover, during spontaneous neutrophil apoptosis, a substantial increase in GALIG gene expression is observed: GALIG still opposes MCL-1. Finally, in bone marrow and peripheral blood cells from patients with Acute Myeloid Leukemia type 2, the level of GALIG transcripts is massively down-regulated when compared to their normal counterparts, while MCL-1 is expressed to the same extent. These data suggest that GALIG could be a key player in the cell death pathway involved in leukocytes homeostasis and myeloid malignancies.
Référence
Mol Immunol. 2013 Nov;56(1-2):123-8
