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. 2015 Sep 2;6(29):27037–27048. doi: 10.18632/oncotarget.4815

Figure 6.

Figure 6

A. Compared with non-CRMAC in Wads−/− mice and normal mucosa in controls, ETV4 and MMP-7 were elevated along with activated ERK pathway in CRMAC of WT mice at week 37 (*P < 0.05). B. Imatinib treatment for 36 hrs inactivated ERK and down-regulated ETV4 in HCT-116 cells in a dose-dependent manner (*P < 0.05, **P < 0.01, ***P < 0.001). C. Imatinib treatment repressed invasion of HCT-116 cells monitored by RTCA. D. Overexpression of c-kit increased phosphorylated ERK and ETV4 in HCT-116 cells in the presence of rhSCF (10 ng/ml) for 36 hrs (*P < 0.05). E. Overexpression of c-kit in the presence of rhSCF (10 ng/ml) enhanced invasive ability of HCT-116 cells recorded by RTCA. F. HCT-116 cells were treated with MEK inhibitor, U0126 (10 μM), for 2 hrs with or without proteosome inhibitor MG132 (20 μM). U0126 treatment significantly inhibited ERK activation and ETV4 expression whereas additional MG132 reversed the decrease of ETV4 (*P < 0.05, **P < 0.01). G. U0126 treatment did not significantly alter mRNA level of ETV4 (P > 0.05).