Fig. 1: PI3K signaling is activated in BCa.
From: Combined Inhibition of PI3K and STAT3 signaling effectively inhibits bladder cancer growth
A Top 30 compounds that induced growth inhibition of 5637 cell. Blue, PIK3/AKT/mTOR inhibitors; Gray, PKC inhibitors; Orange, NF-KB inhibitors; Pink, WNT inhibitors. B Heatmap showed growth inhibition of six bladder cancer cells (5637, J82, UM-UC-3, T24, SW780 and TCCSUP) and one normal urothelial cell line (SV-HUC-1) by indicated pathway inhibitors. C Western blot analysis of phosphorylated and total protein levels of PI3K and AKT in six bladder cancer cells and one normal urothelial cell line. β-actin served as loading controls. D Representative images of phosphorylated PI3K IHC staining in clinical BCa samples (n = 63); PT, para-tumor tissues. Scale bars: (20 μm). E IHC score of phosphorylated PI3K in tumor and matched para-tumor tissues. F Phosphorylated PI3K expression was analyzed based on the clinical stage. G Phosphorylated PI3K expression was analyzed based on the tumor invasion. H GSEA pathway analysis showed PI3K-ATK-mTOR pathway was significantly enriched in the GEO BCa database with tumor tissue, relative to para-tumor tissues. I GSEA pathway analysis exhibited differential gene pathway enrichment in the TCGA BCa datasets with tumor tissue, compared to para-tumor tissues. J Kaplan-Meier analysis of overall survival and recurrence free survival in BCa patients from TCGA based on the expression of PIK3CA mRNA. Red, high PIK3CA mRNA; Black, low PIK3CA mRNA (n = 405). Data are presented as mean ± SD of independent samples with individual data points shown; P values were assessed by two-tailed Student t test in comparison with para-tumor tissues group (E–G).
