Background: Bladder cancer is one of the most common urinary malignancies, and has a high recurrence rate and poor outcomes. In order to identify novel diagnostic and prognostic biomarkers for bladder cancer, we conducted a meta-analysis to analyze the association between long non-coding RNA (lncRNA) expression and survival in bladder cancer. Materials and methods: We searched literature from databases using our inclusion and exclusion criteria. STATA 14.0 software was used to analyze the data from collected studies and to construct the forest plots. A different effect size was selected for each meta-analysis. Results: After selection, 30 articles were found to be eligible. The present meta-analysis contains data from 13 articles about clinicopathological characteristics, six articles about diagnosis, and 16 articles about prognosis. In the present study, we found that many lncRNAs could function as potential diagnostic and prognostic markers in bladder cancer. Among these findings, UCA1 was expected to be a diagnostic biomarker for bladder cancer, while the aberrant expression of HOTAIR and GAS5 was associated with poor disease-free survival/recurrence-free survival/disease-specific survival. Conclusion: Overall, the present study is the first meta-analysis to assess the association between expression of lncRNAs and clinical value in patients with bladder cancer. LncRNAs hold promise as novel diagnostic and prognostic markers in bladder cancer.

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Renal cell carcinoma (RCC) is the most common kidney cancer in adults and has a poor prognosis. cAMP responsive element binding protein 1 (CREB1) is a proto‑oncogenic transcription factor involved in malignancies of various organs. However, its functional role(s) have not yet been elucidated in RCC. We investigated the expression pattern, function and regulation of CREB1 in RCC. CREB1 was overexpressed in the RCC tissues and cell lines. Downregulation of CREB1 inhibited RCC tumorigenesis by affecting cell proliferation, migration and apoptosis. Multiple computational algorithms predicted that the 3'‑untranslated region (3'‑UTR) of human CREB1 mRNA is a target for miR‑10b‑5p and miR‑363‑3p. Luciferase reporter assay, qPCR and western blot analysis confirmed that miR‑10b‑5p and miR‑363‑3p bind directly to the 3'‑UTR of CREB1 mRNA and inhibit mRNA and protein expression of CREB1. qPCR data also revealed a significantly lower expression of miR‑10b‑5p and miR‑363‑3p in RCC tissues. Introduction of miR‑10b‑5p and miR‑363‑3p mimics led to suppressed expression of CREB1 and inhibited cell proliferation, migration and apoptosis reduction. Taken together, we propose that CREB1 is an oncogene in RCC and that upregulation of CREB1 by loss of tumor suppressive miR‑10b‑5p and miR‑363‑3p plays an important role in the tumorigenesis of RCC.

MicroRNAs (miRNAs/miRs) serve an important role in the regulation of carcinogenic pathways. RCC is the most prevalent kidney cancer that occurs in adults. miRNAs have gained increasing attention due to their association with RCC tumorigenesis, serving as biomarkers for early detection and progression monitoring, and as potential targets for molecular therapy. Upregulation of miRNA‑142‑3p has been previously identified in RCC tissues by microarray profile, however, its expression and function in RCC have not yet been validated. In the present study, quantitative polymerase chain reaction was performed to quantify the relative expression of miR‑142‑3p in 53 paired RCC and adjacent normal tissues. Furthermore, wound healing, 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide and flow cytometry assays were performed to analyze the impacts of miR‑142‑3p on cellular migration, proliferation and apoptosis. The results demonstrated that miR‑142‑3p was significantly upregulated in RCC tissues compared with adjacent normal tissues. Downregulation of miR‑142‑3p, induced by chemically synthesized miR‑142‑3p inhibitor, significantly suppressed cell migration and proliferation, and promoted cell apoptosis in 786‑O and ACHN cells, supporting the theory that miR‑142‑3p may function as an oncogene in RCC. The potential clinical significance of miR‑142‑3p, as a biomarker and therapeutic target, provides rationale for further investigation into the miR-142-3p-mediated molecular pathway and how it is associated with RCC development.

Renal cell carcinoma (RCC) is a most common kidney malignancy, with atypical symptoms in the early stage and poor outcome in the late stage. Recently, emerging evidence revealed that some miRNAs play an essential role in the tumorigenesis and progression of RCC. Therefore, the aim of this study is that understand the detailed molecular mechanism of miR-23a-3p in RCC and identify its potential clinical value. In this study, RT-qPCR, wound scratch assay, cell proliferation assay, transwell assay and flow cytometry assay were performed to detect miR-23a-3p expression and its proliferation, migration and apoptosis in RCC. The bioinformatics analysis, RT-qPCR, western blot and luciferase reporter assay were performed to discern and examine the relationship between miR-23a-3p and its potential targets. Moreover, we analyzed the relationship between miR-23a-3p expression and clinicopathological variables or overall survival (OS) from 118 formalin-fixed paraffin-embedded RCC samples. miR-23a-3p is significantly up-regulated in RCC tissue samples, RCC cell lines and the TCGA database. Upregulating miR-23a-3p enhances, while silencing miR-23a-3p suppresses cell viability, proliferation and mobility in ACHN and 786-O cell lines. Besides, overexpression of miR-23a-3p inhibits the cell apoptosis. Then our study further reveals that miR-23a-3p regulates tumorigenesis by targeting Proline-Rich Nuclear Receptor Coactivator 2 (PNRC2). Also, the cox proportional hazard regression analysis indicates that low expression of miR-23a-3p patients has a remarkable longer OS. Our results reveals that miR-23a-3p may not only serve as a new biomarker for prognosis but also serve as a new therapeutic strategy in the RCC treatment.