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. Author manuscript; available in PMC: 2023 Oct 13.
Published in final edited form as: Sci Transl Med. 2023 May 10;15(695):eadf6724. doi: 10.1126/scitranslmed.adf6724

Figure 1. B7-H3(CD276) expression is elevated in tumors with PTEN and TP53 defects.

Figure 1.

(A) Correlation analyses of 53 immune checkpoints with genetic defects of PTEN or TP53 in human prostate tumors (TCGA). Differential expression of immune checkpoints in tumors with PTEN or TP53 defects were analyzed by Student’s t-test, and P values are presented on the X- or Y-axis, respectively. The color indicates the expression (Log2[RNA Seq V2 RSEM+1]) of immune checkpoints in tumors with PTEN or TP53 defects. (B) CD276 mRNA expression in prostate tumors containing PTEN or TP53 defects (TCGA dataset). One-way ANOVA with Tukey’s post hoc tests was performed using GraphPad Prism version 9.2.0..; ∗∗∗∗ P < 0.0001. (C) The CopyKat inferred copy number segmentation identified 14 luminal cell subclones in human prostate tumor samples (Single-cell transcriptional profiling data are from Chen et al., 2021 (41); n=12 patients). (D) The luminal cells were clustered by CD276 expression (left). PTEN and TP53 expression in CD276-low versus -high clusters are shown (right). Differential expression analysis was performed by the Wilcoxon rank-sum test. ∗∗∗∗ adjusted P < 0.0001. (E,F) B7-H3 expression in normal prostate (WT) and prostate tumors from PB-Cre; PtenL/L (PbP) and PB-Cre; PtenL/L; Trp53L/L (PbPP) mice, as determined by qPCR (E) and IHC (F). One-way ANOVA with Tukey’s post hoc tests were performed using GraphPad Prism version 9.2.0.; ∗∗∗∗ P < 0.0001. Scale bar, 100 µm.