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. 2017 Dec 1;9(1):853–865. doi: 10.18632/oncotarget.22856

Figure 3. Gli inhibition and siRNA knockdown reduce EMT and cell cycle activity in EAC cell lines.

Figure 3

(A) Western blots of OE19 and OE33 cells, pretreated with either DMSO (control) or Gli-i (500 nmol/L). Expression of AKT, p-AKT, Snail, Slug, and p21 was examined, with GAPDH serving as a loading control. (B) Western blots of EMT and cell cycle signaling markers in (i) OE19 (Gli1, p-S6K1, ERK, p-ERK, E-cadherin, N-cadherin, Cyclin D1), and (ii) OE33 (Gli1, Gli2, m-TOR, E-cadherin, N-cadherin, β-catenin, Cyclin D1), with GAPDH as a control. Cells were pretreated with DMSO, N-Shh (0.5 mg/mL), Gli-i (500 nmol/L), or Gli-i (500 nmol/L) with N-Shh (0.5 mg/mL) stimulation prior to protein extraction. (C) Western blots of OE19 and OE33 cells, subjected to siRNA treatment. Cells were given control siRNA (100 nM) or Gli1 + Gli2 siRNA (100 nM each) for 48 hours prior to total protein extraction. Expression of Gli1, Gli2, E-cadherin, N-cadherin, and β-catenin was examined, with GAPDH serving as an internal control.