Lu
-ECAM-I is a lung-derived, venular endothelial cell adhesion molecule. It promotes the selective adhesion of lungmetastatic B 16-F I0 melanoma cells to endothelium under static conditions and mediates colonization of the lungs by the same tumor cells. To test whether Lu-ECAM-I by itself is sufficient to cause vascular arrest of B 16-F I 0 cells, we measured here under conditions of flow tumor cell adhesion to endothelia that express different amounts of Lu-ECAM-I on their surfaces. At physiological shear stresses, adhesion of B 16-F 10 melanoma cells to endothelia correlates positively with the amount of Lu-ECAM-I expression on the endothelial cell surface and inversely with the level of the applied shear stress. Tumor cell trajectories are biphasic; i.e., B 16-F I 0 melanoma cells initially move along the endothelial surface with a velocity similar to the theoretical velocity, then arrest within a fraction of a second. Arrest is permanent for most B 16-F I0 melanoma cells at all shear stresses tested. Tumor cells never engaged in a rolling motion prior to arrest. Masking of the Lu-ECAM-I ligand on the surface of B 16-F I 0 melanoma cells with soluble Lu-ECAM-I impedes arrest of tumor cells on the surface of the test endothelium. Purified Lu-ECAM-I also mediates B 16-F I0 arrest, but arrest is mostly transient at shear stresses of 0.59 dynes/cm2 and higher, implying adhesion by single receptor/ ligand bonds. Our data suggest that Lu-ECAM-I plays a critical role in the recognition and initial arrest of murine melanoma cells in lung venules.