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. 2014 Apr 15;289(23):16516–16525. doi: 10.1074/jbc.M113.539031

FIGURE 6.

FIGURE 6.

FAS and FASL are direct targets of GLI1 in pancreatic cancer. A, endogenous GLI1 binds to the fas promoter at regions spanning from −1147 to −943 bp upstream of the first exon. No binding was detected outside this region in an area lacking canonical GLI1-binding site (negative control region/−613 to −486, left panel). Binding of endogenous GLI1 to the fasl promoter at −539 to −293 bp upstream of the first exon. No binding of GLI1 was seen outside this region (negative control region/−1646 to −1517 bp) in this promoter (right panel). B, FAS and FASL mRNA expression in cells overexpressing GLI1 (left panel) or knockdown for GLI1 (right panel). C, reporter assays using the mouse fas and fasl promoters. Cells were cotransfected with the indicated reporter vectors and control or GLI1 expression vectors (left panel) or scramble or shGLI1 vectors (right panel). D, PCNA (proliferation), TUNEL (apoptosis), and DAPI (nuclei). TUNEL staining is positive in KPC pancreas, and fewer areas of apoptosis are noted in GKO/KPC. Proliferation is equal between both cohorts indicating that lack of expression in GKO/KPC is not due to tissue necrosis.