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. Author manuscript; available in PMC: 2014 Feb 15.
Published in final edited form as: Clin Cancer Res. 2013 Jan 23;19(4):809–820. doi: 10.1158/1078-0432.CCR-12-2736

Figure 4.

Figure 4

FGFR4 silencing abrogates the effect of FGF1 on ovarian cancer cell growth and downstream signaling pathway activation. (A) Bar chart showing a significant increase in reporter activity in FGF1-treated OVCA432 cells stably transfected with the Cignal lenti reporter system for the MAPK, NF-κB, and WNT signaling pathways. *P < 0.001. (B) Western blot analysis demonstrating significantly higher level of phosphorylated ERK1/2, GSK-3β, and NF-κB protein in OVCA432 cells treated with FGF1 at 10 ng/mL for 1 hour (+) versus control cells (−). (C) Real-time cell proliferation assay results showing a significantly lower proliferation rate in OVCA432 cells transfected with Hs_FGFR4_5 and Hs_FGFR4_6 than in those transfected with the nontarget scrambled siRNA under treatment with FGF1 at 10 ng/mL (P < 0.001). (D) Bar charts showing the effect of FGF1 on reporter activity, which was significantly lower in ovarian cancer cells transfected with Hs_FGFR4_5 and Hs_FGFR4_6 than in those transfected with the scrambled siRNA (P < 0.001).