Reference : Inverse Expression of Two Laminin Binding Proteins, 67lr and Galectin-3, Correlates with...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
Human health sciences : Oncology
http://hdl.handle.net/2268/24126
Inverse Expression of Two Laminin Binding Proteins, 67lr and Galectin-3, Correlates with the Invasive Phenotype of Trophoblastic Tissue
English
van den Brule, F. A. [> > > >]
Price, J. [> > > >]
Sobel, M. E. [> > > >]
Lambotte, René [Université de Liège - ULg > > Relations académiques et scientifiques (Médecine) >]
Castronovo, Vincenzo mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biologie générale et cellulaire >]
11-May-1994
Biochemical and Biophysical Research Communications
201
1
388-93
Yes (verified by ORBi)
International
0006-291X
[en] Tumor invasion of host tissues and trophoblastic penetration of the endometrium share common biological features. Both processes involve the invasion of basement membranes, an event that is initiated by adhesion of cancer or trophoblast cells to basement membrane components and particularly to laminin. Adhesion to this latter glycoprotein is mediated through a variety of cell surface receptors. We have previously shown that the 67 kD Laminin Receptor (67LR) and a 31 kD Human Laminin Binding Protein, recently renamed galectin-3, are inversely modulated as the invasive phenotype of cancer cells progresses, with up regulation of the former, and down regulation of the latter, respectively. In this study, we examined the expression of these two proteins in 27 human trophoblastic specimens at different gestational ages using Northern and Western blot techniques. Expression of the 67LR increased from 7 weeks to a maximum at 12 weeks, when invasion is maximal, and then decreased. Expression of galectin-3 was inversely modulated by the gestational age, with a minimum expression at 12 weeks. Our data demonstrate that invasive trophoblast displays the same pattern of laminin binding proteins expression than invasive cancer cells, and further demonstrates that invasion of the extracellular matrix by trophoblast and cancer cells share common molecular mechanisms.
BIOMED BMH1-CT92-0520 ; Association contre le Cancer
http://hdl.handle.net/2268/24126

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