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Figure 2 | BMC Cancer

Figure 2

From: Glycogen synthase kinase-3 inhibition disrupts nuclear factor-kappaB activity in pancreatic cancer, but fails to sensitize to gemcitabine chemotherapy

Figure 2

Inhibition of GSK-3 disrupts NF-κB activity in pancreatic cancer cells in a dose-dependent manner. A-B. Western blot analysis of expression of β-catenin and NF-κB target genes: XIAP, BcL-XL, and cyclin D1, in PANC-1 and BxPC-3 cell lines after exposure to AR-18 for 48 h. The change in the expression level of the proteins is compared against untreated or vehicle treated controls. Increase in cytosolic β-catenin level indicates GSK-3 inhibition. Both α-tubulin and β-actin were used as loading controls. C. Effect of GSK-3 disruption on basal and TNF-α induced NF-κB activity measured by luciferase reporter assay. PANC-1 and MIA PaCa-2 cells were exposed to AR-18 (50 μM, 8 h), TNF-α(30 ng/mL, 4 h), or both after co-transfection with TA-LUC NF-κB reporter and β-gal (internal control) constructs. The normalized values are relative to the untreated control (indicating basal level of NF-κB activity) which is represented by dotted line. Each column represents mean for at least four separate experiments, each with three replicates; error bars = ± SEM. (*) significant: (p < 0.0003) when compared to untreated control. (**) significant: (p < 0.0001) when compared to TNF-α treatment.

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