"A. Western blot analysis for <t>pHER2,</t> HER2, pAKT, AKT, pIκBα, IκBα, pNF-κB, NF-κB and netrin-1 in Scr-treated and shMUC4-treated cells, GAPDH was used as a control. B. Western blot analysis for pHER2, HER2 and netrin-1 in Scr-treated and shHER2-treated cells, GAPDH was used as a control. C. Colo-357and Capan-1 cells were treatment with AKT inhibitor for 0h, 3h, 6h and 9h. AKT, pAKT and netrin-1 protein levels were determined by western blot analysis. GAPDH was used as a control. D. Colo-357 and Capan-1 cells were treatment with NF-κB inhibitor for 0h, 3h, 6h and 9h. NF-κB, pNF-κB and netrin-1 protein levels were determinedby western blot analysis. GAPDH was used as a control. E. Schematic representation of the 5′-flanking NTN1 genomic region. Clonedpromoter (shaded box), first exons (black box), NF-κB (p65) binding site, which was identified using the TFSEARCH program, corresponding to nucleotides −307 to −298 (relative to the putative transcription start site +1) F. Scr-treated Colo-357 and shMUC4-treated Colo-357 cells were transfected with pGL3-NTN1 WT or pGL3-NTN1 mutant (preventing NF-κB binding) for 24 h and lysed for the luciferase activity assay. Promoter activity was normalized to pGL3-NTN1WT-transfected Colo-357 Scr cells. The data are presented as mean ± SEM. * p < 0.05. G. Scr-treated Capan-1 and shMUC4-treated Capan-1 cells were transfected with pGL3-NTN1 WT or pGL3-NTN1 mutant (preventing NF-κB binding) for 24 hand lysed for the luciferase activity assay. Promoter activity was normalized to pGL3-NTN1 WT-transfected Capan-1 Scr cells. The data are presented as mean ± SEM. * p < 0.05. H. Western blot analysis for pFAK, FAK, pSrc, Src, pJNK, JNK and MMP9 in Scr-treated and shMUC4-treated cells, GAPDH was used as a control. "