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Functional evidence that cell surface galectin-3 mediates homotypic cell adhesion
1Michigan Cancer Foundation, Department of Pathology and Radiation Oncology, Wayne State University, School of Medicine, Detroit 48201, USA.
Cancer Research
|August 1, 1995
Summary
Cell surface Galectin-3 (Gal-3) mediates tumor cell aggregation during metastasis. This study demonstrates Gal-3
Area of Science:
- Biochemistry
- Cell Biology
- Molecular Biology
Background:
- Galectin-3 (Gal-3) is a beta-galactoside-binding protein implicated in tumor cell metastasis.
- Cell surface Gal-3 is hypothesized to mediate homotypic aggregation of circulating tumor cells.
Purpose of the Study:
- To investigate the role of cell surface Galectin-3 in mediating homotypic cell adhesion.
- To determine if Gal-3 can bridge cells via complementary serum glycoproteins.
Main Methods:
- Recombinant baculovirus encoding Gal-3 was used to infect Sf9 insect cells.
- Immunoblotting and indirect immunofluorescence confirmed Gal-3 expression and localization.
- Cell aggregation assays were performed with and without exogenous glycoproteins and inhibitors.
Main Results:
- Infected Sf9 cells expressed Gal-3 on the cell surface and in the cytoplasm.
- Gal-3-expressing Sf9 cells aggregated in the presence of asialofetuin, a soluble glycoprotein.
- Lactose and anti-Gal-3 antibodies inhibited this aggregation, confirming Gal-3's role.
Conclusions:
- Cell surface Galectin-3 directly mediates homotypic cell adhesion.
- Gal-3 functions by bridging cells through branched, soluble glycoconjugates.
- This mechanism is relevant to tumor cell metastasis.