Reference : The antiangiogenic factor 16K human prolactin induces caspase-dependent apoptosis by a m...
Scientific journals : Article
Human health sciences : Endocrinology, metabolism & nutrition
http://hdl.handle.net/2268/12215
The antiangiogenic factor 16K human prolactin induces caspase-dependent apoptosis by a mechanism that requires activation of nuclear factor-kappa B
English
Tabruyn, Sébastien mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Sorlet, C. M. [> > > >]
Rentier-Delrue, Françoise mailto [Université de Liège - ULg > Département des sciences de la vie > Biologie et génétique moléculaire >]
Bours, Vincent mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Génétique générale et humaine]
Weiner, R. I. [> > > >]
Martial, Joseph mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Struman, Ingrid mailto [Université de Liège - ULg > Département des sciences de la vie > Biologie et génétique moléculaire >]
Sep-2003
Molecular Endocrinology
Endocrine Soc
17
9
1815-1823
Yes (verified by ORBi)
International
0888-8809
Bethesda
[en] We have previously shown that the 16-kDa N-terminal fragment of human prolactin (16K hPRL) has antiangiogenic properties, including the ability to induce apoptosis in vascular endothelial cells. Here, we examined whether the nuclear factor-kappaB (NF-kappaB) signaling pathway was involved in mediating the apoptotic action of 16K hPRL in bovine adrenal cortex capillary endothelial cells. In a dose-dependent manner, treatment with 16K hPRL induced inhibitor kappaB-alpha degradation permitting translocation of NF-kappaB to the nucleus and reporter gene activation. Inhibition of NF-kappaB activation by overexpression of a nondegradable inhibitor kappaB-alpha mutant or treatment with NF-kappaB inhibitors blocked 16K hPRL-induced apoptosis. Treatment with 16K hPRL activated the initiator caspases-8 and -9 and the effector caspase-3, all of which were essential for stimulation of DNA fragmentation. This activation of the caspase cascade by 16K hPRL was also NF-kappaB dependent. These findings support the conclusion that NF-kappaB signaling plays a central role in 16K hPRL-induced apoptosis in vascular endothelial cells.
Giga-Cancer
http://hdl.handle.net/2268/12215

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