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Fig. 6 | Molecular Cancer

Fig. 6

From: Comprehensive characterization of the prostate tumor microenvironment identifies CXCR4/CXCL12 crosstalk as a novel antiangiogenic therapeutic target in prostate cancer

Fig. 6

Single-cell analysis of the endothelial compartment. A Heatmap analysis of the top 10 marker genes of the four EC clusters. Note, the colored arrowheads on the left indicate genes validated by immunohistochemistry (INSRß, FBLN5, Autotaxin (ENPP2)). B Micrographs of immunohistochemistry probing the indicated genes in the tumor vasculature. The left upper panel shows the H&E staining for reference. The left lower p63/AMACR double-staining for PCa validation. C Representation of CXCL12 and CXCR4 expression (y-axis) for each endothelial subtype (x-axis). The statistical significance of the CXCR4/CXCL12 expression difference between the groups was tested using Wilcoxon's test. D Volcano plot of differential analysis of normal vs tumor arterial EC. CXCL12 is indicated in red. E Micrographs of immunohistochemistry probing CXCL12. Note the high expression levels of CXCL12 in the tumor vasculature. F- I. Kaplan–Meier curves and hazard ratio analysis with patients stratified based on the high or low expression of the EC artery signature (F), EC tip marker gene signature (G), EC venous signature (H) and EC immature signature (I). Information from the EC gene expression profiles was condensed into a signature summary using Gene Set Variation Analysis (GSVA). The EC marker gene signature expression cutoff was determined using the results of the GSVA and the R package “maxstat”

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