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To test whether mAb 41-2 also inhibits the arrest of migrating tumor cells in vivo, we first labeled HeLa-CDCP1 cells with green CellTracker and then added them to the CAM blood vessels along with mAb 41-2 or control IgG. On day 5 after inoculation, nonfixed CAM was prepared for confocal fluorescence microscopy. The HeLa-CDCP1 cells are retained in the capillary wall in the absence of mAb 41-2 (Fig. 6A). In contrast, mAb 41-2 is associated with a substantial fraction of the migrating tumor cells (Fig. 6B).

A 3-hour time point showed a few HeLa-CDCP1 cells that had reached the lumen of the capillaries (Fig. 5C). This is the same phenomenon observed in mAb 41-2-treated RCCS1 cells (Fig. 2C). At 6 hours, a substantial fraction of the CDCP1-expressing cells had reached the ends of the capillaries (Fig. 5D). A substantial fraction of these cells were labeled with mAb 41-2 (Fig. 5D, right). In contrast, the CDCP1-negative cells appeared arrested in the narrow spaces of the capillary plexus (Fig. 5D, left). A 3-day time point showed considerable migration of CDCP1-expressing cells across the capillary wall into the chorioallantoic mesenchyme (Fig. 5E, left and right). A substantial proportion of the CDCP1-expressing cells were mAb 41-2 labeled (Fig. 5E, right). These findings showed that a large fraction of the CDCP1-expressing cells can bypass the mAb 41-2-mediated inhibition and arrest in narrow spaces of the capillary plexus. This indicated that the narrow capillary environment is not incompatible with CDCP1 expression and that the binding of 41-2 to CDCP1 results in CDCP1-mediated arrest. These findings explained the arrest in narrow spaces observed in the CAM microvasculature, which is a characteristic feature of CDCP1-expressing tumor cells that comprise a metastasis in vivo. Moreover, these results showed that mAb 41-2 inhibits the ability of CDCP1-expressing tumor cells to metastasize.

For the quantitation of the effects of the CDCP1 mAb 41-2 on tumor cell arrest, the area occupied by living tumor cells was measured in the dorsal CAM 5 days after i.v. inoculation of HeLa-CDCP1 cells in the presence of mAb 41-2 or control IgG. The analysis indicated that the mAb 41-2 treatment significantly reduced tumor cell arrest on the CAM (Fig. 6A). The arrest of HeLa-CDCP1 cells was nearly 100%, compared with 0% for the control IgG-treated group. The quantitation of the tumors, however, was consistent with the above-cited two-hour cell capture data, with only 10% to 20% of the cells escaping mAb 41-2 treatment (Fig. 6B).

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