Reference : Alteration of Interendothelial Adherens Junctions Following Tumor Cell-Endothelial Cell ...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/61990
Alteration of Interendothelial Adherens Junctions Following Tumor Cell-Endothelial Cell Interaction in Vitro
English
Lewalle, J. M. [> > > >]
Bajou, Khalid mailto [Université de Liège - ULg > Département des sciences de la vie > Biologie et génétique moléculaire >]
Desreux, Joëlle mailto [Centre Hospitalier Universitaire de Liège - CHU > > Sénologie >]
Mareel, M. [> > > >]
Dejana, E. [> > > >]
Noël, Agnès mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biologie cellulaire et moléculaire appliquée à l'homme >]
Foidart, Jean-Michel mailto [Université de Liège - ULg > Département des sciences cliniques > Gynécologie - Obstétrique >]
15-Dec-1997
Experimental Cell Research
237
2
347-56
Yes (verified by ORBi)
International
0014-4827
[en] The integrity of the vascular endothelium is mainly dependent upon the organization of interendothelial adherens junctions (AJ). These junctions are formed by the homotypic interaction of a transmembrane protein, vascular endothelial cadherin (VE-cadherin), which is complexed to an intracellular protein network including alpha-, beta-, and gamma-catenin. Additional proteins such as vinculin and alpha-actinin have been suggested to link the VE-cadherin/catenin complex to the actin-based cytoskeleton. During the process of hematogenous metastasis, circulating tumor cells must disrupt these intercellular junctions in order to extravasate. In the present study, we have investigated the influence of tumor cell-endothelial cell interaction upon interendothelial AJ. We show that human breast adenocarcinoma cells (MCF-7), but not normal human mammary epithelial cells, induce a rapid endothelial cell (EC) dissociation which correlates with the loss of VE-cadherin expression at the site of tumor cell-EC contact and with profound changes in vinculin distribution and organization. This process could not be inhibited by metalloproteinase nor serine protease inhibitors. Immunoprecipitations and Western blot analysis demonstrate that the overall expression of VE-cadherin and vinculin as well as the composition of the VE-cadherin/catenins complex are not affected by tumor cells while the tyrosine phosphorylation status of proteins within the complex is significantly altered. Our data suggest that tumor cells modulate AJ protein distribution and phosphorylation in EC and may, thereby, facilitate EC dissociation.
http://hdl.handle.net/2268/61990
10.1006/excr.1997.3799

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