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. Author manuscript; available in PMC: 2014 Jan 9.
Published in final edited form as: Oncogene. 2013 Jan 14;33(2):10.1038/onc.2012.563. doi: 10.1038/onc.2012.563

Figure 7.

Figure 7

sEcad signals through PI3K and MAPK pathways to promote oncogenicity. (a) PAM212 cells were pre-incubated with or without LY294002 (20 μM, PI3K inhibitor) and PD98059 (20 μM, MEK inhibitor) either alone or in combination (20 μM +20 μM) for 1 h, then treated with rmEcadh/Fc (20 μg/mL) for 26h. Cells were lysed, and the indicated proteins were detected by immunoblotting. (b) Proliferation in rmEcad/Fc treated PAM212 cells in the presence or absence of 20 μM PD98059 and 20 μM LY294002, alone or in combination. (c) Migration of rmEcad/Fc-treated PAM212 cells in the presence or absence of LY294002 and PD98059, alone or in combination. (d) Invasion of rmEcad/Fc-treated PAM212 cells with or without pre-incubation of LY294002 and PD98059 alone or in combination. Cells that migrated through the control insert or invaded the Matrigel were fixed, stained, photographed and counted in ten random high-power fields per insert. Results are presented as mean ± SEM of fold change in treated cells compared with control cells. All quantitative data were generated from a minimum of three replicates. (e) Gelatin zymography showing MMP-2 and MMP-9 activities of rmEcad/Fc-treated PAM212 cells with or without pre-incubation of LY294002 and PD98059, alone or in combination.