Fig. 5.

Transcriptomic profiling of 3D-printed model recapitulates prostate cancer proliferation inhibition phenotype observed in human bone metastasis. a) Principal component analysis (PCA) of RNA-seq data from prostate cancer cells in BME versus control conditions. b) Volcano plot of DEGs between BME and control groups. c) GO enrichment of DEGs, highlighting altered biological processes in BME. d) GSEA showing downregulation of mitosis- and proliferation-related GO terms in BME. e) KEGG pathway enrichment analysis of DEGs between BME and control groups. f, g) Heatmaps of DEGs involved in steroid hormone biosynthesis (f) and focal adhesion (g) pathways from KEGG analysis. h) GSEA comparison of Hallmark pathways between BME and control tumor cells. i) GSEA of key regulatory pathways (P53, mitotic spindle, G2M checkpoint, DNA repair) between BME and control. j) Venn diagram showing shared enriched Hallmark pathways between BME vs. control and primary vs. distal tumor cells. k) Sankey diagram illustrating overlap in Hallmark pathway enrichment across comparisons. l, m) Heatmaps of significantly upregulated (l) and downregulated (m) genes from primary and distal tumor cells in BME and control groups. n) Single-sample GSEA (ssGSEA) analysis showing expression trends of top 100 DEGs (by p-value) from primary and distal tumor cells applied to BME and control samples. o) ssGSEA analysis showing expression trends of top 100 DEGs from BME and control tumor cells applied to primary and distal tumor datasets.