Fig. 3

BCL6 suppresses Wnt/β-catenin signaling pathway via directly transcriptionally repressing FZD7. A Volcano plots showed differentially expressed genes (DEGs) (Fold change > 1.5). B Gene ontology (GO) enrichment analysis of BCL6 downstream genes. Wnt signaling pathway was shown to be enriched significantly. C Clustering and heatmap analysis of differential gene expression in the control group and the BCL6 overexpression group in AGS cell. D GEPIA database analysis showed that the expression levels of FZD7 in GC tissues were significantly higher than adjacent non-tumor tissues; KM-plotter database analysis showed that gastric cancer patients with high expression of FZD7 had a worse prognosis (*p < 0.05). E BCL6 could repress FZD7 expression at the transcriptional level in GC cells (***p < 0.001). F Correlations between the immunohistochemical expression of FZD7 and BCL6 in human GC tissues. FZD7 negatively correlates with BCL6 in human GC tissues (N = 137). G Schematic diagram of the FZD7 promoter region and the putative BCL6 binding sites. H, I ChIP analysis of BCL6 binding to the FZD7 promoter in the AGS and SGC-7901 cells. Different regions of the FZD7 promoter contain different putative BCL6 binding sites are shown in G. The matched IgG was used as a negative control and vicinity region (VR) (− 901–0 bp) also used as a control (**p < 0.01, ***p < 0.001). J Luciferase activities of FZD7 promoter reporter vectors in AGS and SGC-7901 cells. Red letters in each binding region indicate the putative or mutated BCL6 binding sequences (**p < 0.01, ***p < 0.001). K β-catenin protein level of GC cells after BCL6 or FZD7 overexpression combined with Wnt inhibitor IWP2 treatment (5 µM, 12 h)