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Accumulating evidence suggest that circRNA RNAs (circRNAs) play important roles in tumor formation and development. circNT5E has been shown to be an oncogenic gene in several types of cancer, and the high expression of circNT5E lead to tumorigenesis and cancer progression. However, the precise role of circNT5E in bladder cancer (Bca) has not been characterized. In this study, we observed that circNT5E expression was augmented in Bca tissues compared with that in adjacent normal tissues, and its expression level was positively associated with larger tumor size and lower survival rate. Further experiments showed that suppression of circNT5E restrained the growth and metastasis of Bca cells in vitro. circNT5E was mainly distributed in the cytoplasm and it captured miR-502-5p to increase HOXC8 mRNA and protein expression. Moreover, decreased miR-502-5p obviously reversed the circNT5E silencing-mediated inhibition of Bca cell growth and migration. Thus, this study suggested that circNT5E may act as a pro-oncogene in the development and progression of Bca and it may become a useful tumor biomarker and promising therapeutic target for Bca treatment.

Purpose The purpose of the present study was to investigate the biological and clinical significance of GATA binding protein 3 (GATA3) in bladder cancer patients. Patients and Methods For the detection of the correlation between GATA3 expression and bladder cancer, we downloaded the mRNA expression data from the Cancer Genome Atlas (TCGA) database and conducted immunohistochemistry staining on formalin-fixed paraffin-embedded (FFPE) sample tissues. Then, bladder cancer cell lines were utilized to investigate the potential functions of GATA3 by cell apoptosis, proliferation and cycle assays. Results The mRNA data from TCGA database and bladder cancer cell lines suggested that GATA3 mRNA expression was significantly higher compared with normal tissues and cells. Conversely, the Western blot assay revealed that the expression of GATA3 was significantly lower in bladder cancer than normal urothelial cell line. Additionally, we found that over-expression of GATA3 was significantly associated with tumor subtype (P = 0.001 in TCGA; P = 0.004 in FFPE tissues), earlier clinical stage (P < 0.001 in TCGA; P < 0.001 in FFPE) and lower grade tumor (P = 0.057 in TCGA; P = 0.002 in FFPE). Kaplan-Meier analysis and multivariate Cox regression analysis indicated that age (P < 0.001 in both cohort), clinical stage (P = 0.028 in TCGA; P = 0.011 in FFPE), recurrence (P < 0.001) and low GATA3 in TCGA cohort (P = 0.035) but high GATA3 in FFPE cohort (P = 0.033) were independent risk factors for overall survival in patients. The assay to detect potential functions of GATA3 indicated that this biomarker could arrest the cell cycle of G2/M and S phase in T24 cells, and inhibit bladder cancer cells proliferation. Conclusion Collectively, our findings identified that GATA3 served as an important prognosis biomarker for bladder cancer patients. However, the mechanism of GATA3 in bladder cancer deserves further studies.

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.

Background Bladder cancer (Bca) is the most common cancer in urinary system. Recent studies revealed that circular RNAs (circRNAs) play vital roles in the development and progression of cancers. circMBOAT2 serves as an oncogenic gene in various kinds of cancer, promoting cell growth and metastasis. Nevertheless, the biological function of circMBOAT2 in Bca has not been reported. Methods qRT-PCR was used to measure the mRNA, circRNA and miRNA expression levels in Bca tissues and cells. Loss-of function experiments were carried to investigate the effect of circMBOAT2 on cell proliferation and migration. Nuclear mass separation, RNA pull-down and dual-luciferase reporter were performed to the molecular mechanisms underlying the functions of circMBOAT2. Results In this research, we identified that circMBOAT2 expression was increased in Bca tissues and positively corelated with unfavorable prognosis. In vitro assay demonstrated that suppression of circMBOAT2 impaired the proliferation and migration of Bca cells. Mechanically, circMBOAT2 was predominantly spread in cytoplasm and it sponged miR-433-3p to strengthen CREB1 expression. Conclusion Hence, our study suggested that circMBOAT2 may serve as an oncogene in the development and progression of Bca and it will be the novel tumor biomarker and therapeutic target for Bca.

O-GlcNAcylation (O-GlcNAc) is a posttranslational modification that is mediated by O-GlcNAc-transferase (OGT) and reversed by O-GlcNAcase (OGA). Increasing evidence indicates that protein O-GlcNAcylation is increased in various types of cancer. In the present study, we aimed to evaluate the expression and function of both OGT and OGA in bladder cancer cells in vitro and in vivo. Expression data of OGT and OGA at the mRNA level was obtained from the Oncomine database. Effects of OGT and OGA on cell proliferate, invasive, and migratory abilities were assessed using MTT, wound healing, cell invasive assay, and cell cycle analysis. In vivo assay was also performed in nude mice. The results revealed that the expression of OGT in bladder cancer tissues was higher than that of normal tissues, while the OGA level was found to be lower in cancer tissues. We also found that knockdown of OGT could inhibit cell proliferation, migration, invasion, and induce cell cycle arrest, while these are reversed when OGA is inhibited. We also observed that O-GlcNAcylation could promote tumor formation in vivo, compared with a negative control. In summary, this study describes the oncogenic role of O-GlcNAcylation in bladder cancer cells.