Fig. 2: ADT-induced EHF depression is important for NE differentiation.
From: Loss of EHF facilitates the development of treatment-induced neuroendocrine prostate cancer
A Bar graph showing EHF expression (left) and heatmap of AR-associated genes including EHF, t-NEPC markers, and an androgen-depressed gene in long-term androgen-deprived LNCaP cells (GSE8702). B, C Effects of androgen deprivation (by culturing in CSS medium) and AR ligand R1881 on EHF expression in LNCaP cells were measured by qPCR and immunoblotting. P values for each sample were obtained based on nontreated controls (*) and cells cultured in CSS medium for 5 days (#) or for 7 days (γ) for EHF and PSA, respectively. D, E Effects of ENZ on EHF expression in C4-2 cells were determined by qPCR and immunoblotting. P values for each sample were obtained based on nontreated controls (*) for EHF and PSA. F EHF, ENO2, and CHGA protein levels in LNCaP cells with/without EHF overexpression responsive to androgen deprivation (by culturing in CSS medium for 48 h) were measured by immunoblotting. G EHF, ENO2, and CHGA protein levels in C4-2 cells with/without EHF overexpression responsive to ENZ treatment for 48 h were measured by immunoblotting. All qPCR and immunoblotting assays were repeated in triplicate. The two-tailed Student’s t test or one-way ANOVA, followed by Dunnett’s t test was used to compare results between two groups with * denoting p < 0.05, **/##/γγ denoting p < 0.01, and ***/###/γγγ denoting p < 0.001. Bar graphs show means ± SD. AAG AR-associated genes, M markers, ADG androgen-depressed gene, AD androgen deprivation, CTL control, CSS charcoal-stripped serum, ENZ enzalutamide, n.s. not significant.
