[Impact of anterior lobe thickness of the prostate on the clinical progression of benign prostatic hyperplasia].

OBJECTIVE: To investigate the correlation of the anterior lobe thickness of the prostate (ALTP) with bladder outlet obstruction (BOO), and evaluate the effect of ALTP on the clinical progression of BPH. METHODS: This retrospective study included 159 cases of BPH. We obtained the clinical indicators of the patients, including ALTP, prostate volume (PV), postvoid residual urine (PVR), maximum urinary flow rate (Qmax), BOO index (BOOI) and IPSS, and analyzed the correlations of ALTP with IPSS, PV, Qmax, age, PVR and BOOI. Using the ROC curve and cut-off point of ALTP, we compared the clinical indicators between the small and large ALTP groups, and analyzed the correlation between ALTP and the clinical progression of BPH. RESULTS: IPSS was not significantly correlated with ALTP (P > 0.05), nor was ALTP with PV and Qmax (P > 0.05). The area under the ROC curve was 0.742 (95% CI: 0.656－0.828) and the cut-off point of ALTP was 0.65 cm. Statistically significant differences were observed in PV, Qmax, IPSS and the rate of surgery between the small ALTP (<0.65 cm) and large ALTP (≥0.65 cm) groups (P < 0.05). CONCLUSION: ALTP is not proportional to PV or to IPSS. ALTP ≥ 0.65 cm increases the incidence of BOO, and may be a risk factor for the clinical progression of BPH.

Upregulation of miR-543-3p promotes growth and stem cell-like phenotype in bladder cancer by activating the Wnt/ß-catenin signaling pathway.

The Wnt/ß-catenin signaling pathway, which is strictly controlled by multiple negative regulators, has been reported commonly hyper activated and closely related to the progression of bladder cancer. However, how tumor cells override the negative regulatory effects to maintain constitutive activation of Wnt/ß-catenin signaling is still unclear. In the current study, we demonstrated that upregulation of miR-543-3p in bladder cancer activated Wnt/ß-catenin signaling by directly targeting Wnt inhibitory factor 1 (WIF1) and Dickkopf 1 (DKK1), which are important antagonist molecules of the Wnt/ß-catenin pathway. Expression of miR-543-3p was upregulated in both bladder cancer tissues and cells, and positively correlated with high-grade bladder cancer. Furthermore, ectopic overexpression of miR-543-3p promoted proliferation and inhibited apoptosis in bladder cancer cells. Notably, overexpression of miR-543-3p enhanced, while silencing miR-543-3p reduced, stem cell-like phenotype of bladder cancer cells. Therefore, our results suggest that miR-543-3p plays a significant role in promoting proliferation and stem cell-like phenotype in bladder cancer, which might be a potential target for anti-bladder cancer therapy.