Fig. 4: HNF1A-AS1 maintains stemness of GCSCs through Wnt/β-catenin pathway.
From: CMYC-initiated HNF1A-AS1 overexpression maintains the stemness of gastric cancer cells

A Western blotting assay was used to identify the effect of HNF1A-AS1 on cancer stemness markers. B, C TOP/FOP-flash reporter plasmid was transfected in GC cells, and luciferase activity was detected (n = 3). D, E qRT-PCR analysis of β-catenin, CMYC, OCT4, SOX2 and NANOG expression in MKN-45 and BGC-823 cells overexpressing HNF1A-AS1 or negative control (n = 3). F, G Immunofluorescence staining assay indicating the localization of β-catenin in GC cells. Confocal micrographs of β-catenin. Original magnification, ×630. H Western blotting assay was used to determine the effect of HNF1A-AS1 on the intracellular localization of β-catenin. I–K The expression of CMYC, OCT4, SOX2 and NANOG in MKN-45 and BGC-823 cells treated with iCRT14 and DMSO were detected by western blotting and qRT-PCR. L, M CCK8 assay to detect cell viability after addition of the Wnt/β-catenin pathway inhibitor iCRT14 (n = 3). Data are representative as the mean ± SD. Two-tailed unpaired Student’s t-test (B–E), one-way ANOVA with Tukey’s multiple-comparison test (J, K), two-way ANOVA test (L, M). *P < 0.05; **P < 0.01; ***P < 0.001.