Fig. 7: Prolonged GC treatment is responsible for ECM remodeling.

A Bulk RNA-Seq analysis and heat map of top 40 significantly regulated genes using PF179T-CAF cells and primary isolated CAFs of 4 PCa patients, after DMSO (control) or 100 nM Dex treatment for 6 d. B Assessment of unique and commonly significantly up- and downregulated GR-target genes, comparing bulk RNA-Seq datasets from PF179T-CAF cells and primary isolated CAFs (fold change ±20%, FDR < 0.05). C GOBP pathway analysis for the identification of significantly regulated pathways after 6 d treatment with 100 nM Dex. D Confirmation of significantly altered GOI mRNA expression of selected ECM and adhesion markers (CLEC3B, CTGF, VCAN, COL8A1, COL7A1, FN1, ITGA10, ITGA8, ITGA7, CLDN7, MMP1, and MMP3) after 6 d treatment with 100 nM Dex or 100 nM Pred using PF179T-CAF cells. Data represent mean + SEM from at least 3 independent experiments (one-way ANOVA and correction for multiple testing using Dunnett’s comparison test; *P < 0.05; **P < 0.01; ***P < 0.001). E Representative IF microscopy images for altered ITGA10 and FN1 protein expression after 6 d 100 nM Dex or 100 nM Pred treatment using PF179T-CAF cells. Magnification: 20x (scale bar = 50 µm). F List of significantly up- or downregulated ECM genes after 6 d GC treatment, which expression corresponds to altered gene expression in primary PCa (TCGA dataset). G Kaplan–Meier analysis for ITGA10 mRNA expression using primary PCa patient data of the TCGA database.