Figure 13.

Analysis of Bcl-xL/BCL2L1 and PPARγ expression in human gastric cancer database. (A) Bcl-xL staining in human GC tissue array. The grade of the Bcl-xL positivity is quantified across the tumor stage (n = 72). (B) Box plot showing the BCL2L1 expression comparing the normal stomach (n = 34) and primary tumor tissue (n = 415) based on the TCGA database. The P value was calculated using a t test. (C) The heat map of the AXIN2, CCND1, LGR5, and SOX9 expression comparing between high- and low- BCL2L1 expressed GC based on the TCGA database (n = 225 vs 225). (D) Sigmoid curve showing the result of the GSEA with gene sets for bile acid and fatty acid metabolism, comparing between high- and low- BCL2L1 expressed GC based on the TCGA database (n = 206 vs 206). (E) Survival analysis of patients with gastric cancer (n = 875) stratified by high vs low BCL2L1 and high vs low PPARG expression. The P value was calculated using a log-rank test. (F) Analysis of Spearman’s rank coefficient between BCL2L1 and PPARG expression (n = 450). (G–J) The analysis of public single-cell RNA sequencing data for GC (GSE239676) comparing tumor epithelial samples with high BCL2L1 expression with those with low BCL2L1 expression (n = 37). (G) Uniform Manifold Approximation and Projection (UMAP) plot colored by GC patient IDs. (H) UMAP plot stratified on the basis of BCL2L1 expression. (I) PCA plot. (J) GSEA with Gene Ontology Biological Process (GOBP) WNT SIGNALING PATHWAY, WP WNT SIGNALING PATHWAY. v2025, GOBP EPITHELIAL CELL PROLIFERATIOHN, and Hallmark bile acid metabolism gene sets and downregulated differentially expressed genes (DEGs) in Hnf4a-OE KPA organoid mice. Scale bars, 100 μm. Mean ± standard error of the mean. ∗P < .05.