Fig. 1: PGE2 non-canonically promotes the Hh pathway activity in colorectal cancer cells.

A, B Luciferase assay for Gli transcriptional activity in colorectal cancer cells with or without PGE2 (1 μM) stimulation. Cells were transfected with GliBS-Luciferase or mGliBS-Luciferase plasmids plus TK-Renilla, and then treated with PGE2 for 6 h (A) or 1–12 h (B). GliBS is a Gli-responsive reporter, and mGliBS is a Gli-unresponsive reporter. Error bars represent SD (n = 3). C Luciferase assay for Gli transcriptional activity in colorectal cancer cells subjected to PGE2 with or without Gli inhibitors As₂O₃ (10 μM), GANT61 (20 μM), and JQ1 (1 μM) for 6 h. Error bars represent SD (n = 3). D The mRNA levels of Gli target genes in colorectal cancer cells were examined by real-time PCR and normalized to the mRNA level of gusb. Cells were exposed to PGE2 (1 μM) with or without As₂O₃ (10 μM), GANT61 (20 μM), and JQ1 (1 μM) for 6 h. Error bars represent SD (n = 3). E The proliferation of colorectal cancer cells was examined with BrdU assays. Cells were exposed to PGE2 (1 μM) with or without As₂O₃ (10 μM), GANT61 (20 μM), and JQ1 (1 μM). Error bars represent SD (n = 3). F Immunoblot analysis of Gli2 expression in LS174T cells transfected with Gli2 siRNA. G The proliferation of colorectal cancer cells LS174T and SW480 was examined with BrdU assays. The cells were transfected with Gli2 siRNA followed by treatment with or without PGE2 (1 μM). Error bars represent SD (n = 3).