A similar effect of the function blocking antibody could result from elimination of potential steric hinderance induced by gal-1, which, however, was not studied here. In an in vitro assay using melanoma cells, recombinant gal-1 increased attachment to laminin in a dose-dependent manner, which could be abolished by lactose and anti-gal-1. In a smooth Staurosporine muscle cell model chemical cross-linking of gal-1 to b1 integrin indicated that dimeric gal-1 bound to a single molecule of b1 integrin and did not cross-link two b1 integrin molecules. Nevertheless, this binding increased the availability of b1 integrin subunits on the cell surface and their activation. By analogy, endogenous cell surface gal-1 of HTR-8/SVneo cells could be bound to b1 integrin and potential further linking of gal-1 ligated membrane and ECM glycoproteins could be achieved by the antibody, possibly activating additional adhesive mechanisms. Gal-1 does not have specific receptors, but possible ligands or counter-receptors include ECM glycoproteins, as well as membrane glycoproteins, such as integrins. Cell column trophoblast cells in vivo and HTR-8/SVneo cells produce ECM proteins including laminin and oncofetal fibronectin. The invasive cytotrophoblast and HTR-8/SVneo cells also express the integrin receptors for these ECM proteins. Both classes of glycoproteins are heavily glycosylated and identified as ligands for gal-1 in several systems and placenta. Therefore, participation of gal-1 in cell adhesion and invasion is likely, possibly through formation of supramolecular structures as has been described for gal-1 on T cells, and other members of the galectin family, such as gal-3. It has been found that gal-1 modulates SB203580 abmole proliferation of different types of cells. The effects of gal-1 on cell proliferation are multifaceted and can be positive or negative, depending on the cell line and/or subcellular localization. The data presented here show increased absorbance in MTT test, suggesting stimulation of cell proliferation in HTR-8/SVneo cells, induced by exogenous recombinant gal-1. This, however, was not accompanied with change in abundance of proliferating or apoptotic cells. In some other responsive cell types gal-1 effects have been dissociated from proliferation and alterations in cell cycle. It has been shown in T cells that gal-1 can support cell survival without promotion of cell proliferation. However, gal-1 isolated from placental tissue inhibited proliferation of choriocarcinoma cell line BeWo cells and reduced cellular uptake of BrdU at concentrations as high as 30 mg/ml and 60 mg/ml. In BeWo cells the signaling cascade of gal-1 at high concentrations is proposed to include receptor tyrosine kinases JAK2, RET and VEGFR3. Apparently, the gal-1 growth promoting effect is cell-type specific, concentration sensitive, and could be both carbohydrate-dependent or – independent. Availability of gal-1 is shown here for the first time to be important for trophoblast invasion in vitro.