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Growing evidence suggests that long non‐coding RNAs (lncRNAs) are associated with carcinogenesis. LncRNA small nucleolar RNA host gene 3 (SNHG3) is up‐regulated in various cancers and positively associated with poor prognosis of these cancers. However, the precise role of lncRNA SNHG3 in bladder cancer (Bca) remains unclear. In our research, we first reported that lncRNA SNHG3 was up‐regulated in bladder cancer tissues and positively related to poor clinical prognosis. Moreover, knockdown of lncRNA SNHG3 significantly suppressed the proliferation, migration, invasion and EMT process of Bca cells in vitro and vivo. Mechanistically, we revealed that suppression of SNHG3 evidently enhanced miR‐515‐5p expression and decreased GINS2 expression at posttranscriptional levels. Moreover, SNHG3 positively regulated GINS2 expression by sponging miR‐515‐5p under a competing endogenous RNA (ceRNA) mechanism. To sum up, our study suggested lncRNA SNHG3 acted as a microRNA sponge and an oncogenic role in the progression of bladder cancer.

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Castration-resistant prostate cancer (CRPC), also known as androgen-independent prostate cancer, frequently develops local and distant metastases, the underlying mechanisms of which remain undetermined. In the present study, surgical specimens obtained from patients with clinical prostate cancer were investigated, and it was revealed that the expression levels of ataxia telangiectasia mutated kinase (ATM) were significantly enhanced in prostate cancer tissues isolated from patients with CRPC compared with from patients with hormone-dependent prostate cancer. CRPC C4-2 and CWR22Rv1 cells lines were subsequently selected to establish prostate cancer models, and ATM knockout cells were established via lentivirus infection. The results of the present study demonstrated that the migration and epithelial-mesenchymal transition (EMT) of ATM knockout cells were significantly decreased, which suggested that ATM is closely associated with CRPC cell migration and EMT. To further investigate the mechanisms underlying this process, programmed cell death 1 ligand 1 (PD-L1) expression was investigated in ATM knockout cells. In addition, inhibitors of Janus kinase (JAK) and signal transducer and activator of transcription 3 (STAT3; Stattic) were added to C4-2-Sc and CWR22Rv1-Sc cells, and the results demonstrated that PD-L1 expression was significantly decreased following the addition of JAK inhibitor 1; however, no significant change was observed following the addition of Stattic. Furthermore, a PD-L1 antibody and JAK inhibitor 1 were added to C4-2-Sc and CWR22Rv1-Sc cells, and it was revealed that cell migration ability was significantly decreased and the expression of EMT-associated markers was effectively reversed. The results of the present study suggested that via inhibition of the ATM-JAK-PD-L1 signaling pathway, EMT, metastasis and progression of CRPC may be effectively suppressed, which may represent a novel therapeutic approach for targeted therapy for patients with CRPC.

Indwelling ureteral stents represent a very frequently used procedure in urological clinical practice that ensures the drainage of urine from the upper urinary tract. However, the stents could result in many stent‐associated complications, such as encrustation and patient discomfort. We developed a new type of biodegradable ureteral stents produced from degradable polyurethane and magnesium alloys. In the present study, we investigated the biocompatibility and the property of degradation of the biodegradable ureteral stents. We evaluated the cytotoxicity of biodegradable ureteral stent by the MTT assay in vitro. The rabbit dorsal muscle embedding test was used to assess the biocompatibility of the degradable stents. Inflammation and fibrosis of muscle tissue were noted to evaluate compatibility at 1, 2, 4, 6 weeks after stents implanted in muscle. The degradation of the biodegradable ureteral stents was assessed by measuring the weight loss of the samples in AUS (artificial urine solution). For validating the degradation property of degradable stents in vivo, we inserted a degradable stent or a conventional biostable stent into Bama pigs. Furthermore, blood studies, liver function tests, renal function tests, urine studies, and computerized tomography (CT) were performed postoperatively. Our study confirms that the degradable polyurethane‐based biodegradable ureteral stent has good biocompatibility. Our biodegradable ureteral stents were completely degraded within 4 weeks and provided a better ability of drainage than conventional stents. They hold promise for decreasing the need for a secondary procedure and stent related morbidity, such as infections.