[Corrigendum] Combination of phospholipase Cε knockdown with GANT61 sensitizes castration‑resistant prostate cancer cells to enzalutamide by suppressing the androgen receptor signaling pathway

Figure 5.

PLCε knockdown suppresses AR expression and nuclear translocation via different signaling pathways. (A) Immunofluorescence demonstrated AR intracellular distribution at 48 h following infection with LV-shPLCε and ad-Gli1/ad-Gli2 in EN-R cells. Magnification, ×400. PLCε knockdown inhibited AR nuclear translocation in EN-R cells. However, the overexpression of Gli-2 reversed the inhibitory effect produced by PLCε. (B) The relative mRNA expression level of Gli-1 and Gli-2 following treatment with an overexpression plasmid of ad-Gli1, ad-Gli2 was examined by RT-qPCR and β-actin served as loading control (NC stands for empty vector plasmid group (*P<0.05, **P<0.01). (C) Protein expression level of Gli-1 and Gli-2 following treatment with the overexpression plasmid of ad-Gli1, ad-Gli2 and PLCε knockdown. (D) The mRNA expression level of Gli-1 and Gli-2 following treatment with overexpression plasmid of ad-Gli1, ad-Gli2 and PLCε knockdown (*P<0.05, **P<0.01). (E) Western blotting showed that PLCε knockdown significantly decreased the AR expression in the nucleus. However, the expression of AR in the nucleus increased following Gli-2 overexpression. (F-H) Western blotting indicated that PLCε knockdown inhibited the PSA expression via the p-STAT3 signaling pathway (The results are represented as the mean ± SD; *P<0.05, **P<0.01 and ***P<0.001). (I and J) Western blotting showed that the downregulation of PLCε decreased the p-STAT3 protein expression in EN-R cells (The results are represented as the mean ± SD; **P<0.01). PLCε, phospholipase Cε; AR, androgen receptor; Gli, glioma-associated homolog; EN-R, enzalutamide-resistant cell line.