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letter
. 2002 Aug 1;87(3):348–351. doi: 10.1038/sj.bjc.6600480

Figure 1.

Figure 1

Effect of β6 suppression, MEK inhibition and deletion of the ERK2 binding site on β6 on MMP-9 secretion. (A) MMP-9 levels in tumour-conditioned medium (TCM) from WiDr and HT29 mock/antisense β6 transfectants. The data represent mean (±s.e.m.) levels of MMP-9 (ng cell−1) for three independent experiments. Asterisks denote statistically significant differences in MMP-9 secretion levels between mock and antisense β6 transfectants for each cell line (P<0.05, Two-sample Wilcoxin rank-sum (Mann-Whitney) test). (B) Gelatin zymogram showing gelatinase activity in TCM from SW480 cells transfected with either the β6 gene construct or with vector alone (mock transfectants). The cells had been exposed to either the MEK-1 inhibitor PD98059 (50 μM) or vehicle control (DMSO) and the position of purified MMP-9 is shown on the left. (C) Gelatin zymogram showing gelatinase activity in TCM from SW480 cells expressing either mutant β6 that lacks the ERK2 binding domain, wild-type β6 or vector alone (mock transfectants). The position of purified MMP-9 is shown on the right.