FIGURE 3.

CXCL12-induced SHH expression in pancreatic cancer cells is dependent on the downstream activation of Akt and ERK. Pancreatic cancer cells (MiaPaCa and Colo357) were pretreated with Akt inhibitor (LY294002, 20 μm) or ERK inhibitor (PD98059, 25 μm) for 1 h, followed by treatment with CXCL12 (100 ng/ml) for either 15 min or 24 h. Total protein was isolated, and expression of Akt, p-Akt, ERK, p-ERK (after 15 min of CXCL12 exposure), and SHH (after 24 h exposure) was examined by immunoblot analysis. β-actin was used as a loading control. Data indicate the selective efficacy of inhibitors and demonstrate that the induction of SHH upon CXCL12 exposure occurs through Akt and ERK pathways.