Fig. 6

CDH4 interrupts the β-catenin–β-TrCP1 interaction and activates the transcription of downstream targets. A IP analyses were performed in TPC-1 and BCPAP cells transiently transfected with His-Mock (pcDNA3.1) or His-CDH4 plasmids, and the abundance of β-TrCP1 in the immunoprecipitates was detected. B IP analyses were performed in PTC cells transfected with CDH4 shRNA or control shRNA. C The effect of CDH4 on β-catenin signaling activity was evaluated by the TOP-flash/FOP-flash luciferase reporter assay. D The RNA level of c-Myc was detected in PTC cells transiently transfected with CDH4-targeting siRNA or control siRNA. E WB analysis of the protein level of c-Myc, MMP7, and VEGF-C in CDH4-silencing PTC cells. F, G TPC-1 (F) and BCPAP (G) cells overexpressing CDH4 were treated with Tegavivint (100 nmol/L, 24 h) as indicated, and qRT-PCR analysis of the RNA level of c-Myc was conducted. H Tegavivint reversed the effect of CDH4 on the expression of c-Myc, MMP7, and VEGF-C. *P < 0.05; **P < 0.01; ***P < 0.01