Fig. 3: FGF18–FGFR2 activate YAP1 expression. | Oncogene

Fig. 3: FGF18–FGFR2 activate YAP1 expression.

From: FGF18–FGFR2 signaling triggers the activation of c-Jun–YAP1 axis to promote carcinogenesis in a subgroup of gastric cancer patients and indicates translational potential

Fig. 3

a The top-ranking geneset enrichments by gene ontology (GO) analysis after rhFGF18 (50 ng/ml) stimulation in MGC-803 cells. b The heatmap demonstrates the differentially expressed genes in the Hippo-YAP1 pathway revealed by RNA-seq. Expressions of crucial genes were validated by qRT-PCR. c The top altered geneset enrichments by GO analysis after FGFR2 knockdown in MGC-803 cells. d The differentially expressed Hippo-YAP1 genes in the siFGFR2 transfectants. Suppression of YAP1 and related genes were validated by qRT-PCR. e rhFGF18 (50 ng/ml) increased YAP1 mRNA expression in a time-dependent manner (*p < 0.05; **p < 0.001). f Western blot analysis indicated the upregulation of YAP1 together with CTGF and N-cadherin after rhFGF18 incubation (50 ng/ml) in all the three cell lines. g Immunofluorescence staining validated the upregulation of YAP1 in AGS and MGC-803 after rhFGF18 stimulation (50 ng/ml; scale bar, 20 μm). h The stimulatory effect induced by rhFGF18 was abolished by FGFR2 knockdown. i The western blot analysis of the upstream components in Hippo-YAP1 pathway. p-LATS1/2 (S909/S872) and p-YAP1 (S127) did not show observable changes after rhFGF18 stimulation. j Tensioned F-actin (green) rearrangement and YAP1 nuclear translocation (red) is triggered by rhFGF18 stimulation (50 ng/ml) but abolished by knocking down FGFR2 in MGC-803 (scale bar, 20 μm). In the statistical bar chart, 1 to 4 represent siScramble + vehicle, siScramble + rhFGF18, siFGFR2 + vehicle, and siFGFR2 + rhFGF18, respectively.

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