Hsa_circ_0074032 promotes prostate cancer progression through elevating homeobox A1 expression by serving as a microRNA-198 decoy.

It has been reported that circular RNA hsa_circ_0074032 (circ_0074032) has a higher level in prostate cancer (PCa) tissues. However, the role and regulatory mechanism of circ_0074032 in PCa are still unknown. Circ_0074032 was overexpressed in PCa, and high circ_0074032 level was associated with worse PCa-related prognosis. Functionally, circ_0074032 silencing decreased xenograft tumour growth in vivo and induced cell apoptosis, curbed cell proliferation, migration and invasion in PCa cells in vitro. Furthermore, circ_0074032 was identified as a miR-198 decoy, and miR-198 inhibition abolished circ_0074032 silencing-mediated effects on PCa cell proliferation, apoptosis, migration and invasion. In addition, miR-198 directly targeted homeobox A1 (HOXA1), and HOXA1 weakened miR-198 mimic-mediated impacts on PCa cell malignant phenotypes. Importantly, circ_0074032 regulated HOXA1 expression by sponging miR-198. Our findings uncovered a novel mechanism by which circ_0074032 promoted PCa progression via elevating HOXA1 expression through acting as a miR-198 sponge, providing a mechanism for circ_0074032 to affect the development of PCa.

Down-regulated LINC00115 inhibits prostate cancer cell proliferation and invasion via targeting miR-212-5p/FZD5/Wnt/ß-catenin axis.

Prostate cancer is the second most frequent malignancy in men worldwide, and its incidence is increasing. Therefore, it is urgently required to clarify the underlying mechanisms of prostate cancer. Although the long non-coding RNA LINC00115 was identified as an oncogene in several cancers, the expression and function of LINC00115 in prostate cancer have not been explored. Our results showed that LINC00115 was significantly up-regulated in prostate cancer tissues, which was significantly associated with a poor prognosis for prostate cancer patients. Functional studies showed that knockdown LINC00115 inhibited cell proliferation and invasion. In addition, LINC00115 served as a competing endogenous RNA (ceRNA) through sponging miR-212-5p to release Frizzled Family Receptor 5 (FZD5) expression. The expression of miR-212-5p was noticeably low in tumour tissues, and FZD5 expression level was down-regulated with the knockdown of LINC00115. Knockdown LINC00115 inhibited the Wnt/ß-catenin signalling pathway by inhibiting the expression of FZD5. Rescue experiments further showed that LINC00115 inhibits prostate cancer cell proliferation and invasion via targeting miR-212-5p/ FZD5/ Wnt/ß-catenin axis. The present study provided clues that LINC00115 may be a promising novel therapeutic target for prostate cancer patients.

Minimally invasive management of acute ureteral obstruction and severe infection caused by upper urinary tract calculi.

PURPOSETo evaluate therapeutic efficacy of two minimally invasive surgical methods in managing acute ureteral obstruction and severe infection caused by upper urinary tract calculi (UUTC).PATIENTS AND METHODSData of 47 patients diagnosed with acute upper urinary tract obstruction and severe infection caused by ureteral calculus using X-ray CT between September 2014 and January 2019 were retrospectively analyzed. All patients were treated with immediate renal drainage and, after infection and ureteral obstruction were relieved, UUTC removal. Renal drainage was performed by ultrasound-guided percutaneous nephrostomy and retrograde ureteral catheterization was performed using cystoscopy. Kidney and ureteral stones were removed; renal function and the urinary tract were examined by X-ray during follow-up.RESULTSPercutaneous nephrostomy was performed in 29 patients in a critical condition including intolerance to surgery, high-grade hydronephrosis, or failure of retrograde ureteric stent placement. In other 18 patients diagnosed with small stones (≤10 mm) and low-grade hydronephrosis, indwelling double-J ureteral stents were temporally installed by a cystoscope. Acute infection and ureteral obstruction were relieved; white blood cell counts returned to normal values within 3 to 7 days after drainage in all patients. In the second-stage treatment, percutaneous nephrolithotomy (PCNL), ureteroscopic lithotripsy, extracorporeal shock wave lithotripsy and nephrectomy were performed in 24, 10, 8 and 5 patients, respectively. No patients developed severe complication after stone removal surgery. All patients were followed up for 3 months to 4.5 years. Renal function was significantly recovered; 17/29 (59%) patients with elevated serum creatinine returned to normal and serum creatinine in 12/29 (41%) patients improved significantly after drainage, with a pre-operation level of 285±169µM vs 203±91µM post-operation (P = 0.014). Five patients were lost during follow-up.CONCLUSIONThis study demonstrated an optimal approach for relieving upper urinary tract obstruction and acute infection in which percutaneous nephrostomy drainage is preferred for patients with severe pyonephrosis, large stones (>10 mm) with high-grade hydronephrosis, steinstrasse, or failure in retrograde ureteric stent placement, while retrograde ureteral catheterization using cystoscopy is suitable for patients diagnosed with small stones (≤10 mm) and low-grade hydronephrosis.

MicroRNA-140 inhibits proliferation and promotes apoptosis and cell cycle arrest of prostate cancer via degrading SOX4.

PURPOSE: To explore the regulatory roles of microRNA-140 and SOX4 in prostate cancer (PCa) tissues and paracancerous tissues, and their underlying mechanism. METHODS: MicroRNA-140 expressions in PCa tissues, paracancerous tissues and PCa cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Proliferation, apoptosis and cell cycle of PCa cells after altering expressions of microRNA-140 and SOX4 were detected by MTT assay and flow cytometry, respectively. The regulatory effect of microRNA-140 on SOX4 was detected by Western blot and qRT-PCR. The binding condition of microRNA-140 on SOX4 was verified by luciferase reporter gene assay. RESULTS: MicroRNA-140 was downregulated in PCa tissues compared to paracancerous tissues. In particular, lower expression of microRNA-140 was found in PCa with Grade I+II compared to Grade III+IV. In vitro, microRNA-140 expression was negatively correlated with proliferative and invasive abilities, while positively correlated with apoptosis of PCa cells. MicroRNA-140 promoted cell cycle arrest in G0/G1 phase. SOX4 expression was inhibited by microRNA-140 overexpression in PCa cells. CONCLUSIONS: Downregulated microRNA-140 promotes proliferation and cell cycle arrest, but inhibits apoptosis of PCa cells. MicroRNA-140 inhibits PCa development via degrading SOX4.