Construction of a risk prediction model for ureteral stricture after ureteroscopic holmium laser lithotripsy.

INTRODUCTION: To analyze the influencing factors of ureteral stenosis after ureteroscopic holmium laser lithotripsy. METHODS: The clinical data of 427 patients treated with ureteroscopic holmium laser lithotripsy were selected, and the patients were divided into two groups based on the presence or absence of ureteral stenosis after the operation. Univariate and multivariate Logistic regression were used to analyze the independent risk factors for postoperative ureteral stenosis, and R software and regression coefficients were used to construct a predictive model. RESULTS: After a one-year follow-up of 427 patients, 28 patients (6.56%) developed ureteral stenosis; univariate analysis showed that the occurrence of ureteral stenosis after subureteral holmium laser lithotripsy was related to stone diameter, stone incarceration, degree of hydronephrosis, holmium laser injury of mucosa, and operation time (P<0.05); further logistic regression analysis showed that a large stone diameter, stone incarceration, and moderate to severe hydronephrosis were independent risk factors for ureteral stenosis after ureteroscopic holmium laser lithotripsy (P<0.05); According to H-L deviation degree and area under ROC curve test, the results show that the model has high accuracy（c2=2.475，P=0.613）and differentiation(0.875(95%CI:0.817-0.919)), and the external verification of the nomogram prediction model was carried out by the verification group. The results showed that the prediction probability of the calibration curve was close to the actual probability and had a good consistency(AUC:0.873 (95CI: 0.822-0.914)). CONCLUSION: The established nomogram model exhibits high accuracy and discriminative ability. It can effectively identify high-risk groups, enabling timely prevention of ureteral stenosis and minimizing the risk of postoperative ureteral stenosis.

n6-methyladenosine-modified circular RNA family with sequence similarity 126, member A affects cholesterol synthesis and malignant progression of prostate cancer cells by targeting microRNA-505-3p to mediate calnexin.

Prostate cancer (PCa) is the most commonly diagnosed malignancy in men. In tumor biology, n6-methyladenosine (m6A) can mediate the production of circular RNAs (circRNAs). This study focused on the mechanism of m6A-modified circRNA family with sequence similarity 126, member A (FAM126A) in PCa. Cell counting kit-8 assay, colony formation assay, 5-ethynyl-2'-deoxyuridine assay, transwell assay, and xenograft mouse models were applied to study the role of circFAM126A in PCa cell growth and tumor metastasis, and cellular triglyceride and cholesterol levels were measured to assess cholesterol synthesis. RNA immunoprecipitation, RNA pull-down, luciferase reporter gene assay, and western blot were adopted to explore the underlying molecular mechanism. Data showed that circFAM126A was upregulated in PCa and promoted PCa progression in vitro. m6A modification of circFAM126A enhanced transcriptional stability. CircFAM126A targeted microRNA (miR)-505-3p to mediate calnexin (CANX). Up-regulating miR-505-3p or inhibiting CANX suppressed cholesterol synthesis and malignant progression in PCa cells. Overexpressing CANX suppressed the inhibitory effect of circFAM126A silencing or miR-505-3p upregulation on PCa cells. Our current findings provide a new therapeutic strategy for the treatment of PCa.

Circular RNA CCT3 is a unique molecular marker in bladder cancer.

This study surveyed circular RNA CCT3 in bladder cancer (BCa). We recruited 85 BCa patients and 40 normal controls (Normal) and collected clinical specimens for analysis. circRNA CCT3 expression was analyzed by RT-qPCR, diagnostic accuracy was calculated by ROC curves, and survival outcomes were evaluated by survival curves. CircRNA CCT3 was overexpressed or knocked down in cells, thereafter to observe the changes in cell malignant phenotypes. The downstream molecules of circRNA CCT3 were detected. Our data suggest that circRNA CCT3 was upregulated in human BCa and was associated with poor survival outcomes of BCa patients. In cell experiments, overexpressing circRNA CCT3 promoted BCa cell malignancy, whereas silencing circRNA CCT3 did the opposite. In addition, circRNA CCT3 modulated PP2A expression by miR-135a-5p. This study demonstrates that circRNA CCT3 is a diagnostic and prognostic biomarker in BCa patients and is a tumor promoter in BCa.

hsa_circ_0003596, as a novel oncogene, regulates the malignant behavior of renal cell carcinoma by modulating glycolysis.

BACKGROUND: This research was planned to analyze hsa_circ_0003596 (circCOL5A1) and glycolysis-focused mechanisms in renal cell carcinoma (RCC). METHODS: circCOL5A1, miR-370-5p, and PRKCSH levels were determined in RCC tissues and selected cell lines by RT-qPCR and/or Western blot. RCC cells after corresponding transfection were tested by colony formation assay, EdU assay, Transwell assay, and flow cytometry to analyze cell proliferation, invasion, migration, and apoptosis. Meanwhile, glycolysis in cells was evaluated by measuring glucose consumption, lactic acid, and ATP production, as well as immunoblotting for HK2 and PKM2. In addition, circCOL5A1 knockdown was performed in animal experiments to observe tumor growth and glycolysis. Finally, the ceRNA network between circCOL5A1, miR-370-5p, and PRKCSH was studied by luciferase reporter assay and RIP experiment. RESULTS: circCOL5A1 and PRKCSH were highly expressed and miR-370-5p was poorly expressed in RCC. circCOL5A1 knockdown depressed RCC proliferation, invasion, migration, and glycolysis, and enhanced apoptosis. circCOL5A1 competitively adsorbed miR-370-5p. Artificial upregulation of miR-370-5p saved the pro-tumor effect of circCOL5A1 on RCC cells, as evidenced by suppression of tumor malignancy and glycolysis. miR-370-5p targeted PRKCSH. PRKCSH overexpression contributed to a reversal of the anti-tumor effect of circCOL5A1 silencing. Silencing circCOL5A1 inhibited RCC tumor growth and glycolysis. CONCLUSIONS: circCOL5A1 regulates the malignant behavior of RCC by modulating glycolysis.