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Figure 7 | Cell Communication and Signaling

Figure 7

From: An increase in integrin-linked kinase non-canonically confers NF-κB-mediated growth advantages to gastric cancer cells by activating ERK1/2

Figure 7

ILK and IQGAP1 facilitate EGF/EGFR-induced NF-κB activation and cell growth and migration, and activated EGFR increases ILK expression. (A) Western blots showing ERK1/2 phosphorylation at Tyr202/Thr204 (pERK1/2) and AKT phosphorylation at Ser473 (pAKT S) in shILK- or siIQGAP1-transfected AGS cells treated with EGF for 1 h. shLuc and control siRNA were used as negative controls. β-actin was used as an internal control. Furthermore, in these cells, NF-κB activation (B), cell growth (C), and migration (D) were detected. Data are mean ± SD from three independent experiments. **P <0.01 and ***P <0.001 compared with negative control. ###P <0.001 compared with shLuc or control siRNA. (E) In EGFR WT-transfected and EGFR VIII-transfected MKN45 cells treated with or without EGF for 1 h plus LY294002 or 17-AAG 24 h posttreatment, western blots show the expression of ILK, phosphorylated ERK1/2 at Tyr202/Thr204 (pERK1/2), and phosphorylated AKT at Ser473 (pAKT S). β-actin was used as an internal control. Upright triangle, increased expression; inverted triangle, decreased expression.

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