Research Article
Cav-1 Ablation in Pancreatic Stellate Cells Promotes Pancreatic Cancer Growth through Nrf2-Induced shh Signaling
Figure 3
Suppression of shh signaling in pancreatic cancer cells abrogates the proproliferative/protumorigenic effects of Cav-1-knockdown PSCs. (a) [3H]Thymidine incorporation assay of Aspc-1 pancreatic cancer cells treated with DMSO or cyclopamine after incubation with CM from PSCs (sh-Ctrl or sh-Cav-1). versus the sh-Ctrl group; # versus the sh-Cav-1 group treated with DMSO. (b and c) Gli-1 and β-actin immunoblot analysis of sh-Ctrl- or sh-Gli-1-transfected Aspc-1 cells before and after treatment with shh. (d) A total of Aspc-1-sh-Gli-1 cells mixed with PSCs with or without Cav-1 knockdown (sh-Ctrl or sh-Cav-1) were implanted subcutaneously in the flanks of BALB/c nude mice ( per group). sh-Ctrl stands for coinjection of Aspc-1 cells and sh-Ctrl-transfected PSC group; sh-Gli-1 stands for coinjection of sh-Gli-1-transfected Aspc-1 cells and sh-Ctrl-transfected PSC group; sh-Cav-1 stands for coinjection of Aspc-1 cells and sh-Cav-1-transfected PSC group; sh-Gli-1+sh-Cav-1 stands for coinjection of sh-Gli-1-transfected Aspc-1 cells and sh-Cav-1-transfected PSC group; tumor volumes were determined by measuring the width and length of the tumors every week. Mean (); bars, SD; Gli-1 knockdown in Aspc-1 cells reversed the tumor-promoting effects of Cav-1-knockdown PSCs, as determined by coinjection experiments. The results are the . per group; , by Tukey’s multiple comparison test.
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