Fig. 5

CARHSP1 promotes the proliferation, migration, and invasion of PCa cells via IL-17RA/STAT3 signaling. (A) GSEA plot revealing a positive correlation between CARHSP1 mRNA levels and the “IL-17 signaling pathway” and “JAK-STAT signaling pathway” in TCGA PCa dataset. (B, C) Expression of CARHSP1, STAT3, p-STAT3, and pathway-related proteins in 22Rv1 and PC-3 cells transfected with shCAR or shCon after adding inhibitor STATTIC (1 μM) for 24 h was detected by western blotting analysis. β-actin was used as a loading control. (D) Western blotting analysis of JAK2, p-JAK2, STAT3, and p-STAT3 in 22Rv1 and PC-3 shCAR cells after treatment with recombinant human IL-17 A (20 ng/mL). β-actin was used as a loading control. (E) Cell viability in 22Rv1 and PC-3 shCAR or shCon cells after treatment with recombinant human IL-17 A at different concentrations for 48 h detected by MTT assay (n = 3, mean ± SD). (F) Cell viability in 22Rv1 and PC-3 shCAR or shCon cells after treatment with recombinant human IL-17 A (50 ng/mL) detected by MTT assay (n = 3, mean ± SD). (G, H) Representative images of the colony formation assay in 22Rv1 and PC-3 shCAR or shCon cells after treatment with recombinant human IL-17 A (50 ng/mL) and quantification analyses of the colony number (n = 3, mean ± SD). (I, J) Representative images of transwell assays and quantification analysis of migration and invasion ability in 22Rv1 and PC-3 shCAR or shCon cells treated as described above (n = 3, mean ± SD). *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant versus the CARHSP1 shRNA group (shCAR). ## p < 0.01 versus the scrambled shRNA group (shCon)