Skip to main content
. Author manuscript; available in PMC: 2016 May 18.
Published in final edited form as: Oncogene. 2015 Sep 14;35(17):2247–2265. doi: 10.1038/onc.2015.288

Figure 8. YAP is required for FGF regulating proliferation and migration of FTSECs.

Figure 8

a) Knockdown of YAP protein with YAP siRNA (siYAP) in FT194 (left panel) and FT246 (right panel) cells eliminate FGF-induced cell proliferation. Each bar represents the mean ± SEM of three independent experiments. Bars with different letters are significantly different from each other (P<0.001). b) Representative images showing that knockdown of YAP with YAP siRNA blocked FGF-induced wound closure in FT194 (left) and FT246 (right) cells. Scale bar = 200μm. quantitative results showing the percentage of wound closure in the wound healing assays in FT194 and FT246 cells was presented in supplementary figure 15. c) RT-PCR results showing that knockdown of YAP with YAP siRNA (siYAP) blocks FGF2-induced expression of AREG mRNA in both FT194 (left panel) and FT246 (right panel) cells. FGF treatments had no effect on YAP and GAPDH mRNA expression. GAPDH was used as an internal control. d) FGF2 stimulates mRNA expression of basic and acidic FGFs in FTSECs. FT246 cells were transfected with non-targeting siRNA (siGLO) or YAP siRNA (siYAP) before treatment with or without FGF2 (10 ng/ml) for 48h. YAP, FGF1 and FGF2 mRNA was detected with RT-PCR. FGF2 stimulates FGF1 and FGF2 mRNA expression, but has no effect on YAP and GAPDH mRNA expression. GAPDH was used as an internal control.