Background
Recent studies have suggested a novel therapeutic strategy for treatment of benign prostatic hyperplasia (BPH) via modulation of autophagy. However, it is not clear whether autophagy induction or inhibition can render better therapeutic efficacy for BPH treatment because autophagy activation in BPH tissue is not precisely known and still contradictory. The
Conclusion
It is suggested that defective autophagy, which is decreased autophagy flux in the prostate gland, may be implicated in BPH, and activating autophagy flux of the prostate with BPH may be used as a potential therapeutic target for treating and alleviating BPH disease.
Methods
We have analyzed and compared autophagic flux which is defined as a measure of autophagic degradation activity in two human prostate epithelial cell lines, RWPE-1 (normal prostate) and BPH-1 (BPH) using LC3-II turnover assay, to clarify the levels of autophagy in BPH.
Results
The in vitro autophagy flux assays showed that autophagy flux was significantly decreased in BPH-1 cell lines compared with RWPE-1 cells under all three conditions of using the original (~62%), the exchanged (~46%), and the same media (Hank's balanced salt solution (HBSS), ~40%), and these results were similar to those seen in the prostate of testosterone-induced BPH rats (~50%) (P < 0.05).