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Vol. 8, Issue 10, 1863-1875, October 1997
2
1
Integrin in Mouse Liver





*Department of Microbiology and Immunology,
§Departments of Oncology and Medical Biophysics,
We report herein that expression of
Transplantation and Immunobiology Group, John P. Robarts
Research Institute, University of Western Ontario, London, Ontario,
Canada
2
1 integrin
increased human erythroleukemia K562 transfectant (KX2C2) cell movement after extravasation into liver parenchyma. In contrast, a previous study demonstrated that
2
1 expression conferred a stationary phenotype to human rhabdomyosarcoma RD transfectant (RDX2C2) cells after extravasation into the liver. We therefore assessed the adhesive
and migratory function of
2
1 on KX2C2 and RDX2C2 cells using a
2
1-specific stimulatory monoclonal antibody (mAb), JBS2, and a
blocking mAb, BHA2.1. In comparison with RDX2C2 cells, KX2C2 were only
weakly adherent to collagen and laminin. JBS2 stimulated
2
1-mediated interaction of KX2C2 cells with both collagen and laminin resulting in increases in cell movement on both matrix proteins. In the presence of Mn2+, JBS2-stimulated adhesion
on collagen beyond an optimal level for cell movement. In comparison,
an increase in RDX2C2 cell movement on collagen required a reduction in
its adhesive strength provided by the blocking mAb BHA2.1. Consistent
with these in vitro findings, in vivo videomicroscopy revealed that
2
1-mediated postextravasation cell movement of KX2C2 cells in the
liver tissue could also be stimulated by JBS2. Thus, results
demonstrate that
2
1 expression can modulate postextravasation
cell movement by conferring either a stationary or motile phenotype to
different cell types. These findings may be related to the differing
metastatic activities of different tumor cell types.
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