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Fig. 5 | Molecular Cancer

Fig. 5

From: A novel AR translational regulator lncRNA LBCS inhibits castration resistance of prostate cancer

Fig. 5

LBCS binds and recruits hnRNPK to AR mRNA to inhibit AR translation in PCa. a RNA pulldown assay was performed using LBCS sense and antisense RNAs incubated with cell lysates of LNCaP cells, followed by silver staining. The red arrow indicates hnRNPK. b The interaction between LBCS and hnRNPK was confirmed by RNA pulldown followed by western blotting in LNCaP and LNCaP-AI cells. c Real time qPCR analysis of LBCS and AR mRNA in RNA immunoprecipitation (RIP) assay of LNCaP and LNCaP-AI cells using anti-hnRNPK, RNA enrichment was determined relative to the non-immuned IgG control. U6 was used as a non-specific control. Lnc-p21 was used as a positive control. The results are presented as the means ± SD of values obtained in three independent experiments. d RIP assay using anti-hnRNPK was performed in either LBCS knockdown or control LNCaP and LNCaP-AI cells, the enrichment of LBCS and AR mRNA was detected by real time qPCR. The results are presented as the means ± SD of values obtained in three independent experiments. e The effect of combined knockdown of LBCS and hnRNPK on the expression of AR in LNCaP cells, as compared with silencing each of LBCS or hnRNPK, or control shRNA, as assessed by western blotting. GAPDH were used as internal control. f The effect of combined overexpression of LBCS and hnRNPK on the expression of AR in LNCaP-AI cells, and the effect of knockdown hnRNPK on AR expression in LBCS overexpressed or control cells. GAPDH were used as internal control. g A schematic model of the mechanism underlying the role of LBCS in castration resistance of prostate cancer. *p < 0.05, **p < 0.01

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