Fig. 5
SLCO4A1-AS1 increased the stability of β-catenin by inhibiting its phosphorylation. a WB analysis showed that siRNA-induced SLCO4A1-AS1 knockdown decreased the protein level of β-catenin in HCT116 and SW480 cells. H3, nuclear marker; EEA1, cytoplasmic marker. b Overexpression of SLCO4A1-AS1 (full-length or nt 900~ 1200) promoted the protein level of β-catenin in HCT116 and SW480 cells. H3, nuclear marker; EEA1, cytoplasmic marker. c Knockdown of SLCO4A1-AS1 enhanced the ubiquitination of β-catenin in HCT116 cells. d SLCO4A1-AS1 knockdown accelerated the degradation of β-catenin in HCT116 and SW480 cells. Chx, cycloheximide. e SLCO4A1-AS1 knockdown promoted the phosphorylation of β-catenin in HCT116 and SW480 cells as shown by western blotting. f WB analysis showed that the protein levels of β-catenin were higher in SLCO4A1-AS1high CRC samples while the phosphorylation of β-catenin was lower. g SLCO4A1-AS1 knockdown enhanced the interaction between β-catenin and GSK3β in HCT116 and SW480 cells. h WB analysis indicated that overexpression of SLCO4A1-AS1 (full-length or nt 900~ 1200) abrogated the interaction between β-catenin and GSK3β in HCT116 and SW480 cells. i, j Restoration of the protein levels of β-catenin by ectopic expression of β-catenin (i) rescued SLCO4A1-AS1 knockdown-induced inactivation of wnt/β-catenin signaling in HCT116 and SW480 cells (j)