Fig. 5
From: A novel lncRNA FLJ promotes castration resistance in prostate cancer through AR mediated autophagy

FLJ promotes autophagy induced by trace androgens via the AR-mediated pathway. A The expression of AR and the autophagy marker LC3B following FLJ knockdown was assessed by WB. B The expression of LC3B, an autophagy marker, after AR activation and inhibition was evaluated by WB. C The fluorescence intensity of LC3B following AR activation and inhibition was measured using immunofluorescence, with a scale bar of 25 μm. D The mean fluorescence intensity of LC3B in C was quantified. E The pathway proteins involved in AR-mediated autophagy induced by trace androgens and their dependency on trace androgens after FLJ knockdown were assessed by WB. F The pathway molecules involved in AR-mediated autophagy induced by trace androgens and their dependency on trace androgens following FLJ knockdown were evaluated by qRT-PCR. G The effect of AR overexpression on LC3B expression and AR-mediated autophagy pathway proteins induced by trace androgens following FLJ knockdown was evaluated by WB. H The effect of AR overexpression on LC3B fluorescence intensity after FLJ knockdown was measured using immunofluorescence, with a scale bar of 25 μm. I The effect of AR overexpression on autophagosomes after FLJ knockdown was evaluated using TEM, with a scale bar of 500 nm. J Quantification of the average fluorescence intensity of LC3B in Fig. 5H. K Quantification of autophagosomes presented in I