Article (Scientific journals)
Restoration of SHIP-1 activity in human leukemic cells modifies NF-kappaB activation pathway and cellular survival upon oxidative stress.
Gloire, Geoffrey; Charlier, Edith; Rahmouni, Souad et al.
2006In Oncogene, 25 (40), p. 5485-94
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Keywords :
Apoptosis/drug effects; Blotting, Western; Cell Survival/drug effects; Flow Cytometry; Genetic Complementation Test; Humans; Hydrogen Peroxide/pharmacology; I-kappa B Kinase/metabolism; I-kappa B Proteins/metabolism; Jurkat Cells; NF-kappa B/metabolism; Oxidation-Reduction; Oxidative Stress; Phosphoric Monoester Hydrolases/genetics/metabolism; Phosphorylation; Reactive Oxygen Species/metabolism; Signal Transduction; Tumor Necrosis Factor-alpha/pharmacology; Vanadates/pharmacology
Abstract :
[en] Nuclear factor-kappa B (NF-kappaB) is an important prosurvival transcription factor activated in response to a large array of external stimuli, including reactive oxygen species (ROS). Previous works have shown that NF-kappaB activation by ROS involved tyrosine phosphorylation of the inhibitor IkappaBalpha through an IkappaB kinase (IKK)-independent mechanism. In the present work, we investigated with more details NF-kappaB redox regulation in human leukemic cells. By using different cell lines (CEM, Jurkat and the subclone Jurkat JR), we clearly showed that NF-kappaB activation by hydrogen peroxide (H2O2) is cell-type dependent: it activates NF-kappaB through tyrosine phosphorylation of IkappaBalpha in Jurkat cells, whereas it induces an IKK-mediated IkappaBalpha phosphorylation on S32 and 36 in CEM and Jurkat JR cells. We showed that this H2O2-induced IKK activation in CEM and Jurkat JR cells is mediated by SH2-containing inositol 5'-phosphatase 1 (SHIP-1), a lipid phosphatase that is absent in Jurkat cells. Indeed, the complementation of SHIP-1 in Jurkat cells made them shift to an IKK-dependent mechanism upon oxidative stress stimulation. We also showed that Jurkat cells expressing SHIP-1 are more resistant to H2O2-induced apoptosis than the parental cells, suggesting that SHIP-1 has an important role in leukemic cell responses to ROS in terms of signal transduction pathways and apoptosis resistance, which can be of interest in improving ROS-mediated chemotherapies.
Disciplines :
Biochemistry, biophysics & molecular biology
Author, co-author :
Gloire, Geoffrey ;  Université de Liège - ULiège > Virologie - Immunologie
Charlier, Edith ;  Centre Hospitalier Universitaire de Liège - CHU > Rhumatologie
Rahmouni, Souad  ;  Université de Liège - ULiège > Département des sciences cliniques > Immunopathologie - Transplantation
Volanti, Cédric
Chariot, Alain ;  Centre Hospitalier Universitaire de Liège - CHU > Chimie médicale
Erneux, Christophe
Piette, Jacques ;  Université de Liège - ULiège > Département des sciences de la vie > Virologie - Immunologie - GIGA-Research
Language :
English
Title :
Restoration of SHIP-1 activity in human leukemic cells modifies NF-kappaB activation pathway and cellular survival upon oxidative stress.
Publication date :
2006
Journal title :
Oncogene
ISSN :
0950-9232
eISSN :
1476-5594
Publisher :
Nature Publishing Group, Basingstoke, United Kingdom
Volume :
25
Issue :
40
Pages :
5485-94
Peer reviewed :
Peer Reviewed verified by ORBi
Available on ORBi :
since 27 January 2009

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