Pin1 positively regulated β-catenin and cyclin D1. (A) β-catenin and cyclin D1 were down-regulated by Pin1 knockdown in CE81T cells. (B) Transactivational potential of β-catenin was reduced in clone 48 cells. Re-expression of Pin1 in clone 48 cells increased the transactivation (top panel). Increased Pin1 and cyclin D1 levels after Pin1 re-expression in clone 48 cells were confirmed (bottom panel). (C) Cell proliferation was attenuated by cyclin D1 knockdown in CE81T cells. (D) In colony forming assay, the colony number was reduced after cyclin D1 knockdown. ** denoted to p <0.01. (E) The inhibited tumorigenesis in clone 48 cells was partially recovered by restoration of cyclin D1 in xenograft tumor model. Ectopic expression of cyclin D1 was confirmed by western blot (bottom panel). (F) Pin1, β-catenin and cyclin D1 in 56 clinical ESCC tumor and corresponding non-tumor tissues were determined. Concomitant upregulation or downregulation of Pin1, β-catenin and cyclin D1 were observed in more than 50% patients.