Nucleolin mediates the antiangiogenesis effect of the pseudopeptide N6L

BMC Cell Biology

Research Article

Josẻ Courty¹  Charalampos Birmpas²  Panagiotis Katsoris²  Jean Paul Briand³ 

[1] CNRS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France;Department of Biology, University of Patras, Patras, Greece;Université Paris Est Créteil, CNRS, Créteil Cedex, France;

关键词: Angiogenesis;    Nucleolin;    Cancer;    N6L;    HB-19;   

DOI  :  10.1186/1471-2121-13-32

 received in 2012-07-31, accepted in 2012-11-04,  发布年份 2012

来源: Springer

【 摘 要 】

BackgroundNucleolin is a protein over-expressed on the surface of activated cells. Recent studies have underlined the involvement of cell surface nucleolin in angiogenesis processes. This cell surface molecule serves as a receptor for various ligands implicated in pathophysiological processes such as growth factors, cell adhesion molecules like integrins, selectins or laminin-1, lipoproteins and viruses. N6L is a synthetic multimeric pseudopeptide that binds cell surface expressed nucleolin and inhibits cell proliferation.ResultsIn the present work, we further investigated the mechanisms of action of pseudopeptide N6L on angiogenesis using HUVECs. We provide evidence that N6L inhibits the in vitro adhesion, proliferation and migration of HUVECs without inducing their apoptosis. In addition, we found that N6L downregulates MMP-2 in HUVECs. The above biological actions are regulated by SRC, ERK1/2, AKT and FAK kinases as we found that N6L inhibits their activation in HUVECs. Finally, down regulation of nucleolin using siRNA demonstrated the implication of nucleolin in the biological actions of these peptides.ConclusionsTaken together, these results indicate that N6L could constitute an interesting therapeutic tool for treating diseases associated with excessive angiogenesis.

【 授权许可】

Unknown   
© Birmpas et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.