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Renal cell carcinoma (RCC) is a common malignant tumor of the urinary system with poor prognosis. microRNAs (miRNAs) are a class of small, non-coding RNA molecules that serve important roles in biological and pathological processes in several types of human tumors. miRNA (miR)-660-5p is dysregulated in many human cancers; however, its role in renal cell carcinoma is currently unclear. In the present study, reverse transcription-quantitative polymerase chain reaction was performed to examine the expression levels of miR-660-5p in RCC tissues and paired normal adjacent tissues (NATs). To determine the function of miR-660-5p in RCC cells, wound-healing and Matrigel assays were performed to determine the effects of miR-660-5p on cell migration and invasion, respectively. MTT and Cell Counting kit-8 assays were performed to determine the effects of miR-660-5p on RCC cell proliferation. In addition, flow cytometric analysis was performed to validate the effects of miR-660-5p on apoptosis. The results indicated that miR-660-5p expression was downregulated in RCC tissues compared with NATs. Restoration of miR-660-5p expression using synthetic mimics may suppress cell migration, invasion and proliferation, and induce cell apoptosis, while using synthetic inhibitors may promote cell migration, invasion and proliferation, and suppress cell apoptosis. These results suggested that miR-660-5p may serve a tumor suppressive role in RCC tumorigenesis. [ABSTRACT FROM AUTHOR]

Highlights: [•] Hsa-miR-125b and SIRT7/MALAT1 are inversely expressed in bladder cancer. [•] Hsa-miR-125b inhibits bladder cancer cell growth and motility, and increases apoptosis. [•] Hsa-miR-125b downregulates oncogene SIRT7 in bladder cancer. [•] Hsa-miR-125b downregulates oncogenic long non-coding RNA MALAT1 in bladder cancer. [•] Hsa-miR-125b suppresses bladder cancer development via inhibiting SIRT7 and MALAT1. [Copyright &y& Elsevier]

Highlights • MiR-31-5p is downregulated in RCC tissues and cell lines. • miR-31-5p downregulation was associated with poor prognosis in RCC patients. • Overexpression of miR-31-5p inhibited RCC cell proliferation, migration and invasion and cell cycle. • CDK1 is the novel target gene of miR-31-5p. Abstract Background: Renal cell carcinoma (RCC) accounts for more than 90% of cancers in the kidney. RCC is often asymptomatic, as a result people with RCC generally have advanced disease by the time it is discovered and has a poor prognosis compared to other cancers. Therefore, it is necessary to explore its pathogenesis and identify some reliable prognostic biomarker of RCC. miRNAs are emerging as important players in the development and progression of RCC. miR-31-5p has been reported to act as a tumor suppressor in hepatocellular carcinoma (HCC). The aim of this study is to determine the detailed molecular mechanism of miR-31-5p in the progression of RCC and to investigate its potential clinical value. Methods: In this study, RT-qPCR, EdU assay, CCK-8 assay, wound scratch assay, transwell assay, flow cytometry assay and cell cycle assay were performed to detect miR-31-5p expression and its functions in RCC. Moreover, 42 formalin-fixed paraffin-embedded (FFPE) RCC samples were used to analyze the relationship between miR-31-5p expression and patients' overall survival. Finally, luciferase reporter assay, RT-qPCR assay and western blot were used to explore the association between miR-31-5p and its potential targets. Results: miR-31-5p was significantly down-regulated in RCC tissues and RCC cell lines compared with paired adjacent normal tissues and normal cell lines. miR-31-5p downregulation was associated with poor prognosis in RCC patients. Overexpression of miR-31-5p inhibited RCC cell proliferation, migration and invasion and cell cycle. Conversely, down-regulation of miR-31-5p promoted cell proliferation, migration and invasion. Furthermore, cyclin-dependent kinasec1 (CDK1), a key player in cell cycle regulation, was identified as a functional target of miR-31-5p. Conclusions: Our results suggest that miR-31-5p serves as a tumor suppressor in RCC and is expected to be a molecular biomarker for poor prognosis of RCC. [ABSTRACT FROM AUTHOR]

Background MicroRNA(miRNA) plays a key regulatory role in various stages of tumorigenesis, including cell growth, cell cycle control, apoptosis avoidance, tissue invasion, and metastasis. Several microRNAs are involved in the development of renal cell carcinoma (RCC) and the malignant transformation process. However, the effects of miR-663a on RCC have rarely been reported. Methods In the present study, the expression of miR-663a was examined in RCC using matched normal kidney tissues and four cell lines (786-O, Caki-1, ACHN and HK-2). MicroRNA mimics were transiently transfected into RCC cells and the effects of over expression on proliferation, migration, invasion, and apoptosis was observed. In addition, the relationship between miR-663a expression in 42 formalin-fixed paraffin-embedded (FFPE) clear cell renal carcinoma (ccRCC) samples and clinical pathological variables and overall survival was investigated. We evaluated the prognostic value of miR-663a expression in ccRCC by experimental results. Results The results showed that the expression of miR-663a was up-regulated in RCC cells and tissues and miR-663a was associated with proliferation, migration, invasion, and apoptosis of RCC. Cox proportional hazard regression analysis showed that a high expression of miR-663a patients had a significantly shorter overall survival in univariate and multivariate analysis. Kaplan-Meier survival curves showed that a high expression of miR-663a patients had a significantly shorter overall survival. Conclusions These results indicate that miR-663a can be used as an independent marker for the poor prognosis of ccRCC, and may also play an important role as a tumor oncogene in the occurrence and development of RCC. [ABSTRACT FROM AUTHOR]