Figure 8.
(A) MCF-10A cells were plated for 48 hr in the presence of 50 μg/ml control antibody, 25 μg/ml P1B5 (an α3 integrin-inhibitory antibody), 25 μg/ml P1B5 on RTC-coated wells, 25 μg/ml GoH3 (an α6 integrin-inhibitory antibody), a 1:250 dilution of an inhibitory antibody against FN, and a 1:50 dilution of P1E6 (an α2 integrin-inhibitory antibody). At 48 hr the cells were trypsinized and counted. To confirm that the anti-FN antibody and P1E6 are function-inhibiting in our hands, we undertook adhesion assays in which 2 × 105 MCF-10A cells and OVCA429 cells were plated onto either FN- or RTC-coated wells of a 96-well plate (B). (B) Left panel, the anti-FN antibody inhibits the attachment of MCF-10A to the FN-coated wells by 37%. Right panel, P1E6 inhibits the adhesion of OVCA429 cells to RTC by 49%. The latter confirms the results of Moser et al. (1996). The SDs indicated in the graphs in B were determined from the data derived from three trials. (C) MCF-10A cells were plated into medium containing 50 μg/ml control antibody, 50 μg/ml RG13 antibody, or 50 μg/ml RG13 antibody together with a 1:5 dilution of hybridoma medium containing the β1 integrin-activating antibody TS2/16.2.1 or 50 μg/ml 3E1 antibody. As in A, at 48 hr the cells were trypsinized and counted. In A and C, % Proliferation indicates the increase in cell number as a percentage of that observed in the control antibody-treated cell population. In A and C, the control cell population expanded from 2 × 104 to 1.025 × 105 or from 2 × 104 to 1.18 × 105 after 48 hr (100%).