Recently, accumulating studies demonstrate that some long non-coding RNAs (lncRNAs) contain open read frames and have protein/peptide-coding potential. NCYM is a 109-amino acid product encoded by lncRNA MYCNOS variant 2 that is an antisense transcript of MYCN oncogene. NCYM is amplified in human neuroblastomas and associated with poor prognosis. However, its functional role in Wilms tumor (WT) remains unclear. In this study, we identified lncRNA MYCNOS as a promising prognostic factor in Wilms tumor through bioinformatics analysis. The expression of NCYM and downstream genes was determined by western blotting. Cell proliferation, migration, and invasion were measured by CCK-8, wound healing and Transwell assays, respectively. Cell apoptosis was evaluated by flow cytometry assay. The subcutaneous xenograft and lung metastasis mouse model were established by the armpit injection or tail intravenous injection of WT cells, respectively. Our results showed that NCYM was validated to be abundantly expressed in Wilms tumor cell lines and tissues. The exogenous overexpression of NCYM promoted WT cell proliferation, migration, and invasion. The silencing of SIX1 expression abolished the pro-growth effect of NCYM and downregulated β-catenin in WT. Additionally, NCYM facilitated tumor growth and formation of lung metastasis in vivo. In summary, the exogenous overexpression of NCYM could play a critical role in WT progression by mediating SIX1 and β-catenin as an oncopromoting factor.

To analyze the heterogeneity between different cell types in pediatric Wilms tumor (WT) tissue, and identify the differentially expressed genes (DEGs) of malignant tumor cells, thereby establishing a prognostic model. The single-cell sequencing data of pediatric WT tissues were downloaded from the public database. Data filtration and normalization, principal component analysis, and T-distributed stochastic neighbor embedding cluster analysis were performed using the Seurat package of R language. Cells were divided into different clusters, malignant tumor cells were extracted, and DEGs were obtained. Then, the pseudo-time trajectory analysis was performed. Prognostic biomarkers were determined by univariate and multivariate COX regression analyses and LASSO regression analysis. Kaplan–Meier survival analysis and receiver operator characteristic curve analysis were performed. Combined with the prognostic biomarkers and clinical characteristics, a nomogram was generated to predict WT prognosis. The prognostic power was validated in the external datasets. Cells in the WT tissue were divided into 10 clusters. Three prognostic biomarkers that affected the survival time of patients were screened from 215 DEGs in malignant tumor cells, and a nomogram was constructed using the three genes and clinical characteristics. The area under the curve (AUC) values of 3- and 5-year disease-free survival were 0.756 and 0.734, respectively. In the external validation dataset, the AUC value of this nomogram model was 0.826. Based on the single-cell RNA-seq, we recognized cell clusters in the WT tissue of children, identified prognostic biomarkers in malignant tumor cells, and established a comprehensive prognostic model. Our findings might provide new ideas and methods for the diagnosis and treatment of WT.

BACKGROUND:Circular RNA (circRNA) has been shown to play an essential role in cancer progression, including nephroblastoma. Hsa_circ_0093741 was discovered to be highly expressed in nephroblastoma. However, its function and mechanism in nephroblastoma development are still vague.METHODS:The expression levels of hsa_circ_0093741, miR-562 and FRS2 (Fibroblast Growth Factor Receptor Substrate 2) were detected using western blotting and quantitative real-time polymerase chain reaction. Functional experiments were performed by using cell counting kit-8, colony formation, 5-ethynyl-2'-deoxyuridine (EdU), transwell, scratch assays in vitro and animal experiments in vivo. The interaction analysis was conducted using dual-luciferase reporter assay and RIP assay.RESULTS:Hsa_circ_0093741 was highly expressed in nephroblastoma tissues and cells. Functionally, hsa_circ_0093741 silencing significantly suppressed the growth, invasion, and migration of nephroblastoma cells in vitro. MiR-562 was decreased in nephroblastoma, and was validated to be a target of hsa_circ_0093741. Inhibition of miR-562 reversed the anticancer functions of hsa_circ_0093741 silencing on nephroblastoma cells. FRS2 expression was increased in nephroblastoma and served as a target of miR-562, moreover, FRS2 overexpression attenuated the inhibitory functions of miR-562 on the nephroblastoma cell malignant phenotypes mentioned above. Pre-clinically, lentivirus-mediated hsa_circ_0093741 silencing also impeded nephroblastoma tumor growth and metastasis in vivo.CONCLUSION:Knockdown of hsa_circ_0093741 suppresses nephroblastoma cell growth, migration and invasion by regulating the miR-562/FRS2 axis, suggesting the potential involvement of hsa_circ_0093741 in nephroblastoma progression.

The aim of the present case report was to investigate the clinical features, pathological examination and treatment of eosinophilic cystitis (EC) in children. Two cases of EC were reported and reviewed from January 2016 to March 2017. Case 1 (male; 6 years old) had intermittent hematuria, frequent urination, urgent urination, difficulty in urination and abdominal pain. Case 2 (male; 7 years old) had frequent urination, urgent urination, urinary pain, dysuria and suprapubic pain with no hematuria. One patient had a history of allergies and both patients underwent a cystoscope biopsy. Blood eosinophils were clearly increased and a bone marrow biopsy examination revealed that marrow eosinophils were also increased in both cases. The urine culture results were negative. Ultrasonography and computed tomography revealed uneven thickening of the bladder wall and diffusive mucosal lesions. Cystoscopy revealed that the bladder volume became smaller and the mucosa at the bladder floor and neck was red. Lesions were biopsied through the urethra and the following characteristics were observed: Congestion and edema of the bladder mucosa, infiltration of the blood vessels and eosinophils in the muscular layer, accompanied by focal muscle necrosis. Patient 1 was administered anti-inflammatory and cetirizine hydrochloride treatments, followed by 6 weeks of prednisone dose-reduction therapy. Patient 2 was administered antibiotics and cetirizine hydrochloride. Following 6-month follow-ups, abnormal voiding symptoms had disappeared in each case. Ultrasonography and computed tomography revealed no bladder wall thickening or space-occupying lesions. EC in children is rare and easily misdiagnosed as nonspecific bladder inflammation or bladder occupying lesions. Cystoscopy and biopsy are necessary to diagnose EC and conservative treatments with anti-inflammatory, anti-allergic and cortical hormone nonspecific treatments are suggested.