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Renal cell carcinoma (RCC) is the most common type of malignant tumor of the adult kidney and has a poor prognosis. MicroRNAs (miRs) are important in a wide range of biological and pathological processes, including cell differentiation, migration, growth, proliferation, apoptosis and metabolism. The present study aimed to determine the role exerted by miR-30a-5p in the tumorigenesis of RCC. The expression levels of miR-30a-5p in RCC tissues and RCC-derived cells were demonstrated to be significantly downregulated by real-time quantitative polymerase chain reaction (RT-qPCR). Wound scratch assay, cell proliferation assay and flow cytometric analysis revealed that the abilities of migration and proliferation of the RCC-derived cells were suppressed, whereas cell apoptosis was promoted, when miR-30a-5p was overexpressed in these cells. N-acetylgalactos aminyltransferase 7 (GALNT7) was predicted to be one target gene of miR-30a-5p by bioinformatics analysis. Luciferase reporter assay, RT-qPCR and western blotting were performed to confirm that GALNT7 is the direct conserved target of miR-30a-5p. These results suggested that miR-30a-5p has a tumor-suppressive role in the tumorigenesis of RCC. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is the most common type of kidney cancer in adults, which is associated with poor prognosis and high recurrence. Long non-coding RNAs (lncRNAs) have been reported to be dysregulated in cancer and to be important in the regulation of carcinogenesis, thus suggesting that this class of molecules may be used as biomarkers in cancer. The lncRNA urothelial carcinoma associated 1 (UCA1) has been observed to be upregulated and tofunction as an oncogene in certain types of cancer; however, the role of UCA1 in RCC remains to be elucidated. The present study aimed to determine the expression and function of UCA1 in RCC. Quantitative polymerase chain reaction (qPCR) was used to determine the expression levels of UCA1 in 46 paired RCC and adjacent normal tissue samples. Furthermore, qPCR was used to determine the expression levels of UCA1 in four RCC cell lines compared with the human embryonic kidney 293T cell line. The impact of UCA1 on cell migration, proliferation and apoptosis was investigated by wound scratch assay, MTT and flow cytometry, respectively. The results of the present study demonstrated that UCA1 expression levels were significantly increased in RCC tissues and cells, as compared with the controls. Ectopic expression and gene silencing of UCA1 in RCC cell lines exerted opposite effects on cellular proliferation, migration and apoptosis, and the results suggested that UCA1 may function as an oncogene in RCC. These results indicated that UCA1 may be considered as a promising biomarker for diagnosis, and a therapeutic target in RCC. Further research is required to elucidate the role and target genes of UCA1 in RCC. [ABSTRACT FROM AUTHOR]

Clear cell renal cell carcinoma (ccRCC) is the predominant and most aggressive type of kidney malignancy, however, the mechanism underlying its carcinogenesis remains to be elucidated. The present study aimed to determine the expression and function of microRNA (miR)-429 in ccRCC carcinogenesis. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-429 in ccRCC specimens. Following transfection of miR-429 synthetic mimics, the expression of miR-429 was examined and cell proliferation, cell migration, apoptosis and luciferase assays were conducted in ccRCC cell lines. The results demonstrated that expression of miR-429 was decreased in ccRCC cells. In addition, upregulation of miR-429 by transfection of mimics reduced cellular proliferation and migration, and induced apoptosis in ACHN and 786-0 cell lines. Furthermore, miR-429 decreased the 3'UTR luciferase activity of vascular endothelial growth factor (VEGF) and c-MYC, and RT-qPCR analysis demonstrated that the cancer cells transfected with miR-429 mimics exhibited decreased expression of VEGF, but not c-MYC. To the best of our knowledge, the present study was the first to reveal that downregulated miR-429 functioned as a tumor suppressor by restraining cellular proliferation and migration, and inducing apoptosis, as well as targeting VEGF in ccRCC cells. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is the most common type of renal tumor, which has a poor prognosis. Improvements in understanding the underlying molecular biology of RCC has led to systemic treatments, which have markedly improved patient outcomes. Therefore, it is necessary and worthwhile to identify novel biomarkers for RCC. MicroRNAs (miRNAs) have been found to be important in a wide range of biological and pathological processes, including cell differentiation, migration, growth, proliferation, apoptosis and metabolism. Aberrant expression of miRNA-130b has previously been reported in tumors, however, its role in RCC remains to be elucidated. In the present study, the upregulation of miR-130b was observed in RCC tissues and cell lines using reverse transcription-quantitative polymerase chain reaction analysis, which was consistent with previous microRNA profiling in RCC. Furthermore, the effects of miR-130b on cell migration, proliferation and apoptosis were examined using a wound scratch assay, an MTT assay and flow cytometric analysis, respectively. The results demonstrated that the downregulation of miR-130b by a synthesized inhibitor inhibited cell migration, suppressed cell proliferation and induced RCC cell apoptosis. The present study was the first, to the best of our knowledge, to suggest that miR-130b may be a promising biomarker for diagnosis and a therapeutic target for the treatment of RCC. Further investigations are required to examine the roles and target genes of miR-130b in RCC. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is the most common type of kidney cancer in adults and is associated with a poor prognosis due to a lack of early-warning signs, protean clinical manifestations, and resistance to radiotherapy and chemotherapy. Recently, increasing evidence has suggested that microRNAs (miRNAs) are involved in the proliferation, invasion and apoptosis of various types of human cancer cells. In a previous study, miRNA expression profiles from renal cell carcinoma (RCC) revealed that expression of miR-20b-5p was significantly downregulated in RCC tissues. The aim of this study was to investigate the expression and functional significance of miR-20b-5p in RCC. The expression of miR-20b-5p was quantified in 48 paired RCC tissues and cell lines, and compared with adjacent normal tissues and the 293T cell line by reverse transcription-quantitative polymerase chain reaction. The functional impact of miR-20b-5p on cell proliferation, cell migration and apoptosis in the 786-O and ACHN RCC cell lines, was determined by an 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide assay, a scratch assay and flow cytometry. To the best of our knowledge, the present study was the first to reveal that miR-20b-5p was downregulated in RCC tissues and cell lines. It also demonstrated that upregulation of miR-20b-5p inhibited cellular migration and proliferation, and promoted cellular apoptosis, suggesting that miR-20b-5p functioned as a potential tumor suppressor. However, further studies are required to fully determine the effects of miR-20b-5p and the miR-20b-5p-mediated molecular pathway in RCC and other types of cancer. In conclusion, these results imply that miR-20b-5p may be a biomarker for early detection and prognosis prediction, as well as a therapeutic target for RCC. [ABSTRACT FROM AUTHOR]

Kidney cancer is the 14th most common cancer in the world and its prognosis remains poor due to difficult early detection and treatment. Therefore, the identification of biomarkers for early-stage renal cell carcinoma (RCC) is important. MicroRNA-106b (miR-106b) has been described as an oncogene in several types of human cancer. Previous microarray studies have suggested that miR-106b was significantly upregulated in RCC tissues compared with paired normal kidney tissues and may be a promising biomarker for the prediction of early metastasis following nephrectomy. The present study aimed to determine the expression and function of miR-106b in RCC. The expression of miR-106b in RCC tissues and cells, and in paired normal tissues and cells was determined by reverse transcription quantitative polymerase chain reaction, based on the previous sequencing results of miRNAs. Furthermore, a wound scratch assay, MTT assay and flow cytometry were performed to examine the functions of miR-106b on cell migration, proliferation and apoptosis. The results demonstrated that miR-106b was upregulated in RCC tissues and cell lines compared with control normal tissues and cell lines. Downregulation of miR-106b with a synthesized inhibitor suppressed cell migration and proliferation and induced renal cancer cell apoptosis, suggesting that miR-106b can be characterized as an oncogene in RCC. To the best of our knowledge, the present study was the first to reveal that miR-106b is upregulated and affects cellular migration, proliferation and apoptosis in RCC. Further studies are required to examine the role and target genes of miR-106b in RCC. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) have been demonstrated to exhibit abnormal expression patterns in various types of human cancer. The aim of the present study was to identify a novel tumor suppressor microRNA (miR) and investigate its physiological function and mechanism in renal cell carcinoma (RCC). The expression levels of miRNA (miR)-362-3p expres were measured in 47 pairs of RCC and adjacent normal tissue samples, using reverse transcription-quantitative polymerase chain reaction analysis. In addition, miR-362-3p was transfected into renal cancer cells to investigate its role in the regulation of cell proliferation, migration, invasion, apoptosis and cell cycle. Identification of the target gene of miR-362-3p was performed using luciferase reporter assays and western blot analyses. The results demonstrated that the expression levels of miR-362-3p were downregulated in the RCC tissue samples, compared with the adjacent normal tissue samples. The upregulation of miR-362-3p using a synthesized mimic suppressed the proliferation, migration and invasion of the renal cancer cells, and induced cell apoptosis and G1 phase arrest. Further experiments demonstrated that the overexpression of miR-362-3p resulted in decrease expression levels of nemo-like kinase. These results suggested that miR-362-3p functions as a tumor suppressor in RCC, and may serve as a potential molecular target in the treatment of RCC. [ABSTRACT FROM AUTHOR]

MicroRNA (miR)-510-5p has been demonstrated to be involved in a number of types of malignancy; however, the function of miR-510-5p in renal cancer remains unclear. The present study aimed to determine the expression of miR-510-5p in renal cell carcinoma (RCC) specimens and analyzed the impact of miR-510-5p on renal cancer by 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide, wound scratch and apoptosis assays. The results showed that miR-510-5p was significantly downregulated in RCC specimens compared with normal renal specimens. Overexpression of miR-510-5p by synthetic mature mimics reduced cell proliferation and migration and induced an increase in cell apoptosis, indicating that miR-510-5p may act as a tumor suppressor in RCC. The present study firstly revealed that downregulated miR-510-5p functioned as a tumor suppressor by reducing cellular proliferation and migration, and inducing apoptosis in RCC. Further research is required to define target genes of miR-510-5p to determine the cellular mechanism of miR-510-5p in the carcinogenesis of RCC. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRs) are small, endogenous noncoding RNAs that serve a significant function in various biologic processes, including those involved in cancer. The present study aimed to determine the expression and function of miR-16 in renal cell carcinoma (RCC). Quantitative polymerase chain reaction was used to quantify the expression of miR-16 in 48 paired RCC tissues and adjacent normal tissues. The impact of miR-16 on cell proliferation, migration and apoptosis was analyzed by transfecting miR-16 mature molecules into the renal cancer cell lines 786-O and ACHN. The results indicated that miR-16 was significantly upregulated in RCC tissues (P<0.05). Downregulation of miR-16 resulted in reduced cell proliferation and migration and increased levels of apoptosis, while overexpression of miR-16 resulted in accelerated cellular proliferation and migration, suggesting that miR-16 may function as an oncogene in RCC. The present study demonstrated for the first time, to the best of our knowledge, that miR-16 is upregulated in RCC and acts as an oncogene by inducing cellular proliferation, migration and reducing apoptosis. Further study of miR-16 in RCC may clarify the molecular mechanisms of RCC carcinogenesis and aid in the development of novel biomarkers and therapeutic options. [ABSTRACT FROM AUTHOR]

miR-125a-5p has been previously described as a tumor suppressor in numerous malignancies, however the expression and function of miR-125a-5p in renal cell carcinoma (RCC) remains to be elucidated. In the present study, to explore the potential role of miR-125a-5p in RCC, quantitative polymerase chain reaction was used to determine the expression levels of miR-125a-5p in renal cancer tissues. The influence of miR-125a-5p on cell proliferation, migration and apoptosis was also determined, using an MTT assay, a wound scratch assay and flow cytometry, respectively. The expression of miR-125a-5p was shown to be decreased in RCC and the restoration of miR-125a-5p by synthetic mimics was shown to suppress cell proliferation and migration, and induce apoptosis. The present results indicate that miR-125a-5p may function as a tumor suppressor in RCC. The present study is, to the best of our knowledge, the first to demonstrate the downregulation of miR-125a-5p in RCC, and to show the role it has in affecting cellular proliferation, migration and apoptosis. Further research is needed to define the target genes of miR-125a-5p and explore the potential of miR-125a-5p as a diagnostic or a prognostic biomarker for RCC. [ABSTRACT FROM AUTHOR]