Fig. 2: DPYSL5 expression is suppressed by AR. | Communications Biology

Fig. 2: DPYSL5 expression is suppressed by AR.

From: DPYSL5 is highly expressed in treatment-induced neuroendocrine prostate cancer and promotes lineage plasticity via EZH2/PRC2

Fig. 2

a Enzalutamide (ENZ) induces DPYSL5 mRNA expression along with NEPC markers, NSE in LNCaP, and (b) NSE, SYP, and ASCL1 in C42B cells. c Silencing AR expression with siRNA (siAR) in LNCaP and C42B cells increases DPYSL5 expression based on qPCR analysis. Bars represent mean ± SD with n = 3. p-values shown as asterisks (*p ≤ 0.05, **p ≤ 0.01 and ***p ≤ 0.001). d AR ChIP-seq data from LNCaP and C42B cells stimulated with DHT. A putative AR binding site in the second intron of DPYSL5 gene with a sequence of 5’-TACACATTTTGTTGG-3’ is highlighted. e AR binding to the DPYSL5 gene was verified using AR-DPYSL5 qPCR-ChIP. f The effect of R1881 on DPYSL5 mRNA levels in LNCaP and in LNCaP EnzR cells (expression compared to LNCaP cells grown with FBS) and in C42B and in C42B EnzR cells (expression compared to C42B cells grown with FBS) and (g) on protein level (R1881 = synthetic androgen methyltrienolone, CSS=charcoal stripped serum). h DPYSL5 is highly expressed in AR-negative, NE-positive LuCaP xenografts and (i) patient tumor samples in Labreque et al. 2019 dataset. j Neurite lengths and (k) branch points in ENZ-resistant (EnzR) and parental LNCaP and C42B cells calculated using IncuCyte NeuroTrack analysis software module. l Comparison of the cellular ultrastructures of LNCaP, LNCaP EnzR, C42B and C42B EnzR cells using scanning electron microscopy.

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