Reference : The angiostatic 16K human prolactin overcomes endothelial cell anergy and promotes le...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/13844
The angiostatic 16K human prolactin overcomes endothelial cell anergy and promotes leukocyte infiltration via nuclear factor-kappaB activation
English
Tabruyn, Sébastien mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Sabatel, Céline mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Nguyen, Ngoc-Quynh-Nhu mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Verhaeghe [> >]
Castermans, Karolien mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Malvaux, Ludovic mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Griffioen, A. W. [> > > >]
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 > GIGA-R : Biologie et génétique moléculaire >]
2007
Molecular Endocrinology
Endocrine Society
21
6
1422-9
Yes (verified by ORBi)
International
0888-8809
Chevy Chase
MD
[en] Angiostatic Proteins/*pharmacology ; Animals ; Cell Adhesion ; Clonal Anergy/*drug effects/genetics ; Endothelium, Vascular/*drug effects/immunology ; Gene Expression/*drug effects ; Humans ; Leukocytes/drug effects/immunology ; Melanoma, Experimental/genetics/immunology/pathology ; Mice ; NF-kappa B/genetics/*physiology ; Oligonucleotide Array Sequence Analysis ; Peptide Fragments/*pharmacology ; Prolactin/*pharmacology ; Skin Neoplasms/genetics/immunology/pathology
[en] The 16-kDa N-terminal fragment of human prolactin (16K hPRL) is a potent angiostatic factor that inhibits tumor growth in mouse models. Using microarray experiments, we have dissected how the endothelial-cell genome responds to 16K hPRL treatment. We found 216 genes that show regulation by 16K hPRL, of which a large proportion turned out to be associated with the process of immunity. 16K hPRL induces expression of various chemokines and endothelial adhesion molecules. These expressions, under the control of nuclear factor-kappaB, result in an enhanced leukocyte-endothelial cell interaction. Furthermore, analysis of B16-F10 tumor tissues reveals a higher expression of adhesion molecules (intercellular adhesion molecule 1, vascular cell adhesion molecule 1, or E-selectin) in endothelial cells and a significantly higher number of infiltrated leukocytes within the tumor treated with 16K hPRL compared with the untreated ones. In conclusion, this study describes a new antitumor mechanism of 16K hPRL. Because cellular immunity against tumor cells is a crucial step in therapy, the discovery that treatment with 16K hPRL overcomes tumor-induced anergy may become important for therapeutic perspectives.
Giga-Cancer
http://hdl.handle.net/2268/13844
2007/04/05

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