ORBi: Viatour Patrick - NF-kappa B2/p100 induces Bcl-2 expression

Reference : NF-kappa B2/p100 induces Bcl-2 expression


	Document type :	Scientific journals : Article
	Discipline(s) :	Human health sciences : Hematology Human health sciences : Oncology
	To cite this reference:	http://hdl.handle.net/2268/2971

Title :	NF-kappa B2/p100 induces Bcl-2 expression
Language :	English
Author, co-author :	Viatour, Patrick [Université de Liège - ULg > > Chimie médicale >]
	Bentires-Alj, Mohamed [> > > >]
	Chariot, Alain [Université de Liège - ULg > Département de pharmacie > Chimie médicale >]
	Deregowski, Valérie [> > > >]
	de Leval, Laurence [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Anatomie et cytologie pathologiques >]
	Merville, Marie-Paule [Université de Liège - ULg > Département de pharmacie > Chimie médicale >]
	Bours, Vincent [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Génétique générale et humaine]
Publication date :	Jul-2003
Journal title :	Leukemia
Publisher :	Nature Publishing Group
Volume :	17
Issue/season :	7
Pages :	1349-1356
Audience :	International
ISSN :	0887-6924
City :	London
Keywords :	[en] NF-kappa B ; Bcl-3 ; Bcl-2 ; oncogene ; apoptosis ; cancer
Abstract :	[en] The NF-kappaB2/p100 and bcl-3 genes are involved in chromosomal translocations described in chronic lymphocytic leukemias (CLL) and non-Hodgkin's lymphomas, and nuclear factor kappaB (NF-kappaB) protects cancer cells against apoptosis. Therefore, we investigated whether this transcription factor could modulate the expression of the Bcl-2 antiapoptotic protein. Bcl-2 promoter analysis showed multiple putative NF-kappaB binding sites. Transfection assays of bcl-2 promoter constructs in HCT116 cells showed that NF-kappaB can indeed transactivate bcl-2. We identified a kappaB site located at position -180 that can only be bound and transactivated by p50 or p52 homodimers. As p50 and p52 homodimers are devoid of any transactivating domains, we showed that they can transactivate the bcl-2 promoter through association with Bcl-3. We also observed that stable overexpression of p100 and its processed product p52 can induce endogenous Bcl-2 expression in MCF7AZ breast cancer cells. Finally, we demonstrated that, in breast cancer and leukemic cells ( CLL), high NF-kappaB2/p100 expression was associated with high Bcl-2 expression. Our data suggest that Bcl-2 could be an in vivo target gene for NF-kappaB2/p100.
Research units :	Giga-Signal Transduction
Funders :	FNRS, TELEVIE, FBC, ARC ULG
Target :	Researchers ; Professionals ; Students
Permalink :	http://hdl.handle.net/2268/2971

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