Fig. 8: FOXA2 expression in AR-dependent PCa cells initiates a multilineage progression.
From: FOXA2 rewires AP-1 for transcriptional reprogramming and lineage plasticity in prostate cancer
a, b Immunoblotting for indicated proteins in LNCaP cells stably expressing empty vector or FOXA2 (LN-FOXA2-OE) (a) or in NCI-H660 cells transfected with siFOXA2 versus siNTC (b) (n = 3 independent experiments). c qRT-PCR for indicated FOXA2 targets in the control LNCaP versus LN-FOXA2-OE cells (n = 3 independent samples, data are represented as mean ± SEM, statistical significance determined by unpaired two-sided t-test). d, e Cell proliferation assay (d) or transwell migration assay for the control LNCaP versus LN-FOXA2-OE celIs (e) (n = 3 independent samples, data are represented as mean ± SEM, statistical significance determined by unpaired two-sided t-test). f GSEA for the pathways (HALLMARK and PID datasets) enriched in the upregulated genes by FOXA2 overexpression. g Box plots for subtype-specific transcriptional signatures (n = 93 genes for every subtype) in the control LNCaP versus LN-FOXA2-OE ceIls (center: median; box: 25th–75th IQR; whiskers: 1.5x IQR; outliers: individual data points; statistical significance determined by unpaired two-sided t-test). h Heatmap view (left panel) and reads density plot (right panel) for FOXA2 or JUN binding peak intensity centered at previously defined chromatin sites with different ATAC signatures in LN-FOXA2-OE cells. ns (P > 0.05), *(0.01 < P < 0.05), **(0.001 < P < 0.01), ***(P < 0.001), and ****(P < 0.0001) were used to indicate the levels of P-value. Source data are provided as a Source Data file.
