title: Opposing Mcl-1, the GALIG proapoptotic gene is upregulated as neutrophils die and underexpressed in Acute Myeloid Leukemia cells.
abstract: 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.
authors.affiliation: Centre de Biophysique Moléculaire, CNRS UPR 4301, affiliated with the Université d'Orléans-Pôle Universitaire Centre Val de Loire, Orléans, France. lucile.mollet@cnrs-orleans.fr
authors.forename: Lucile
authors.initials: L
authors.lastname: Mollet
authors.forename: Pauline
authors.initials: P
authors.lastname: Robinet
authors.forename: Martine
authors.initials: M
authors.lastname: Dubois
authors.forename: Axel
authors.initials: A
authors.lastname: Aurouet
authors.forename: Thierry
authors.initials: T
authors.lastname: Normand
authors.forename: Stéphane
authors.initials: S
authors.lastname: Charpentier
authors.forename: Adelin
authors.initials: A
authors.lastname: Sureau
authors.forename: Camille
authors.initials: C
authors.lastname: Grandclement
authors.forename: Francine
authors.initials: F
authors.lastname: Garnache-Ottou
authors.forename: Eric
authors.initials: E
authors.lastname: Deconinck
authors.forename: Fabienne
authors.initials: F
authors.lastname: Brulé
authors.forename: Pierre Simon
authors.initials: PS
authors.lastname: Rohrlich
authors.forename: Alain
authors.initials: A
authors.lastname: Legrand
mesh_terms: D017209:Apoptosis / Q000235:genetics*; D001798:Blood Proteins / Q000235:genetics* / Q000378:metabolism; D001854:Bone Marrow Cells / Q000378:metabolism; D002470:Cell Survival / Q000235:genetics; D037161:Galectins / Q000235:genetics* / Q000378:metabolism; D015973:Gene Expression Regulation, Leukemic; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D006367:HeLa Cells; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008856:Microscopy, Fluorescence; D064549:Myeloid Cell Leukemia Sequence 1 Protein; D009504:Neutrophils / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D001798:Blood Proteins; D037161:Galectins; C428445:LGALS3 protein, human; D064549:Myeloid Cell Leukemia Sequence 1 Protein; D019253:Proto-Oncogene Proteins c-bcl-2; D049452:Green Fluorescent Proteins