Fig. 3

Effects of serine protease inhibitors on wound closure. At 100nM subtilisin promotes the closure of a scratch wound in MCF-7 cultures between 0 h and 72 h relative to the closure rate in untreated cells (a, b). The quantified scratch closure data are summarised in chart (c). The effect of subtilisin at 30 and 100nM is shown on the expression of (d) neogenin, (e) unc-5C, (f) RhoA in the same cell line of MCF-7 breast adenocarcinoma cells. Chymotrypsin (1 μM) shows a similar ability to facilitate wound closure (g, h) as summarised in panel (i). Chymotrypsin has a similar but weaker action on neogenin expression (j) without affecting unc-5C (k) or RhoA (l). In separate experiments (m) the rate of wound closure is again facilitated by subtilisin (n) whose effect is blocked by the chymotryptic protease inhibitor chymostatin (o, p). Similarly the Bowman-Birk inhibitor from soybean was able to completely block the facilitation of cell migration produced by chymotrypsin (q-t). Bars represent mean ± s.e.mean of the percentage change in wound area (n = 3–4). **P < 0.01; ***P < 0.001 relative to the control bar. Calibration bars: 200 μm