Fig. 5: FGF18–FGFR2 regulates YAP1 expression through c-Jun. | Oncogene

Fig. 5: FGF18–FGFR2 regulates YAP1 expression through c-Jun.

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. 5

a FGFR2 knockdown inhibited FGFR and c-Jun phosphorylation in GC cells. b rhFGF18 stimulation promoted FGFR and c-Jun phosphorylation, but the effect was attenuated by FGFR2 depletion. c Two putative binding sites of c-Jun on the YAP1 promoter region (2000 bp upstream of YAP1 transcription starting site). d ChIP-qPCR analysis revealed the enrichment of c-Jun on YAP1 promoter in MGC-803 cells. IgG was applied as negative control and data normalized by input (**p < 0.001). c-Jun enrichment abolished by FGFR2 knockdown//. e The knockdown of JUN decreased mRNA and protein expression of YAP1 in GC cells (**p < 0.001) as well as the YAP1 downstream targets, CTGF, and c-Myc. f Immunoprecipitation of the YAP1/TEAD4 complex was determined by western bot in MGC-803 with siScramble, siFGFR2, or siJUN transfection, respectively. IgG was applied as a negative control. g GC cell proliferation was inhibited by JUN knockdown (**p < 0.001). h The impaired monolayer colony formation by JUN depletion (**p < 0.001). i YAP1 re-expression rescued the impaired monolayer colony formation caused by JUN knockdown in AGS and MGC-803 cells (**, siJUN vs. siScramble, p < 0.001; ##, siJUN vs. siJUN + YAP1, p < 0.001). j Cell invasive ability was suppressed by JUN knockdown but reversed by ectopic expression of YAP1 (**, siJUN vs. siScramble, p < 0.001; ##, siJUN vs. siJUN + YAP1, p < 0.001) (scale bar, 50 μm). k siJUN and siYAP1 increased the first-line anti-cancer drug (5-FU) sensitivity. IC50 was shown accordingly.

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