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Micro (mi)RNAs are involved in multiple cellular processes, and alterations in miRNA expression have been demonstrated to lead to tumorigenesis. Previous microarray analysis revealed that miRNA (miR)-24 was downregulated in renal cell carcinoma (RCC). Additionally, miR-24 has been identified as an oncogene and tumor suppressor in various cancers. The present study assessed the expression levels of two stem-loops of miR-24, miR-24-1 and miR-24-2, in RCC tissues and paired healthy tissues by reverse transcription-quantitative polymerase chain reaction. The results revealed that miR-24-2 was upregulated in RCC tissues and ACHN, 786-O and 769P cell lines compared with healthy tissues and HEK-293T cells, respectively, whereas miR-24-1 was almost absent in RCC and healthy kidney tissues. To investigate the role of miR-24-2 in RCC, a synthesized miR-24-2 mimic, negative control (NC), inhibitor or inhibitor NC was transfected into 786-O and ACHN RCC cells, and cell proliferation, mobility and apoptosis assays were performed. The results of the present study revealed that miR-24-2 was associated with cell proliferation, migration, invasion and apoptosis, thus demonstrating that miR-24-2 may serve a role as an oncogene in RCC. Further studies are required to investigate the signaling pathways of miR-24-2, and the potential of miR-24-2 as a therapeutic target or biomarker for the early detection of RCC. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is the most common type of kidney cancer, and the prognosis of metastatic RCC remains poor with a high rate of recurrence and mortality. A previous study has revealed that microRNA (miRNA), which negatively regulates protein expression, serves a role of oncogene or tumor suppressor. The aim of the present study was to investigate the expression and function of miR-514a-3p in RCC. To detect the expression of miR-514a-3p in 32 paired RCC tissues, quantitative polymerase chain reaction (qPCR) was performed. The function of miR-514a-3p in the proliferation, mobility and apoptosis of RCC cells (786-O and ACHN) was assessed by MTT, CCK-8, cell scratch, Transwell, Hoechst 33342 staining and flow cytometry assay. The results of qPCR revealed that miR-514a-3p was signifi- cantly downregulated in RCC tissues compared with adjacent normal tissues. Upregulation of miR-514a-3p by transfection of mimics suppressed RCC cell proliferation, migration and invasion, and induced cell apoptosis. The results revealed that miR-514a-3p was significantly downregulated in RCC and may serve a role as tumor suppressor in RCC. Further studies are required, focusing on the possibility of using miR-514a-3p as a biomarker for RCC as well as the pathway of miR-514a-3p in RCC. [ABSTRACT FROM AUTHOR]

The long non-coding RNA (lncRNA) urothelial carcinoma associated 1 (UCA1) is an oncogenic lncRNA in bladder cancer, and its upregulation is associated with enhanced cell invasion. However, the underlying mechanism remains to be elucidated. The present study demonstrated that UCA1 was positively associated with cell invasion ability and promoted epithelial-mesenchymal transition (EMT) of bladder cancer cells by inducing high mobility group box 1 (HMGB1). Furthermore, bioinformatics and luciferase reporter assays demonstrated binding sites of the tumor suppressive miR-143 within UCA1 and the 3'untranslated region of HMGB1. UCA1 negatively regulated miR-143 expression in a dose-dependent manner in bladder cancer cells. In addition, UCA1 and HMGB1 were upregulated and miR-143 was downregulated in bladder cancer specimens. Overall, the data suggested that UCA1 may promote the invasion and EMT of bladder cancer cells by regulating the miR-143/HMGB1 pathway, which exhibits an important regulatory role in the pathology of bladder cancer. [ABSTRACT FROM AUTHOR]

As influencing factors of genesis and progression in several types of human tumor, microRNAs (miRs) serves roles in the regulation of tumor cell viability, migration, and apoptosis. The present research aimed to investigate the association between the function of miR‑100‑5p and renal cell carcinoma (RCC). miR‑100‑5p expression was determined in RCC tissue and paired normal tissue samples using reverse transcription‑quantitative polymerase chain reaction. To assess the effects of miR‑100‑5p on cell viability, migration and apoptosis, multiple methods were used, including scratch wound assays, MTT assays, and flow cytometry. It was demonstrated that miR‑100‑5p was significantly upregulated in RCC tissue compared with in normal adjacent tissue samples. Furthermore, the viability and migration of 786‑O and, ACHN cells tranfected with miR‑100‑5p was significantly increased compared with the negative control group. In addition, miR‑100‑5p‑transfected 786‑O and ACHN cells demonstrated significantly reduced cellular apoptotic rates compared with the negative control group. To the best of our knowledge, the present study is the first to report an association between miR‑100‑5p and RCC. The results of the current study suggest that tumor oncogene miR‑100‑5p could be used as a diagnostic biomarker for RCC. [ABSTRACT FROM AUTHOR]

In recent years, accumulating evidence has demonstrated that microRNAs (miRs, miRNAs) may serve an important role in the occurrence and development of tumors. miR-23a-5p has been confirmed as an oncogene in numerous diseases through gene chip analysis. However, as the most common type of renal tumor, the expression and function of miR-23a-5p in renal cell carcinoma (RCC) remains unclear. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis, and Cell Counting Kit-8 (CCK-8), wound scratch, Transwell, MTT and flow cytometry assays were performed to investigate the role of miR-23a-5p in RCC. The expression of miR-23a-5p in RCC tissue samples was significantly higher compared with that in normal tissue samples (P<0.01). Furthermore, the expression of miR-23a-5p in RCC cell lines (786O, ACHN and Caki-1) was significantly higher compared with that in the human embryo kidney 293T cell line, as determined using RT-qPCR (P<0.001). In addition, the results revealed that the upregulation of miR-23a-5p promoted the proliferation, migration and invasion of RCC cells, and inhibited RCC cell apoptosis. The downregulation of miR-23a-5p resulted in the reversal of the results described above. Additionally, it was observed that the downregulation of miR-23a-5p significantly promoted ACHN and 786O cell viability (P<0.001). The results of the present study suggest that miR-23a-5p is an oncogene in the occurrence and development of RCC and may be a novel therapeutic target for RCC. [ABSTRACT FROM AUTHOR]

There is increasing evidence that the deregulation of microRNAs (miRNAs; miRs) contributes to tumorigenesis. Previous studies have shown that miR-195 is downregulated in various types of cancer. The present study aimed to investigate the function and expression levels of miR-125b. Results of qPCR revealed that miR-195-3p, the mature sequence of miR-195, was upregulated in renal cell carcinoma (RCC) tissues and cell lines (786-O, 769P and ACHN). This indicated that the function and role of miR-195-3p may differ in different types of tumor. To assess the function of miR-195-3p in RCC cell lines, cell proliferation was examined using MTT and CCK-8 assays, mobility was assessed using a cell scratch assay, Transwell migration assay and invasion assay, and apoptosis was examined using flow cytometry. These assessments were also performed in cells with upregulated or downregulated miR-195-3p via transfection with synthesized miR-195-3p mimic or inhibitor. The results revealed that the overexpression of miR-195-3p promoted 786-O and ACHN RCC cell proliferation, migration and invasion, and inhibited cell apoptosis, whereas the downregulation of miR-195-3p suppressed cell proliferation, migration and invasion, and induced cell apoptosis. These results indicated that miR-195-3p was associated with the tumorigenesis of RCC, with further investigations to focus on the pathway and use of miR-195-3p as a clinical biomarker for RCC. [ABSTRACT FROM AUTHOR]

microRNAs (miRs) have been investigated as a novel class of regulators of cellular processes, including proliferation, apoptosis and metabolism. In particular, miR-30b has been demonstrated to be deregulated in certain types of cancer, including lung, colorectal and gastric cancer. Previous studies of miR-30b in renal clear cell carcinoma demonstrated that the expression level of miR-30b was associated with distant metastasis. However, the function of miR-30b in renal cell carcinoma (RCC) remained to be elucidated. In the present study, the expression of miR-30b in 31 paired RCC tissues from four cell lines (786-O, 769-P, ACHN and 293T) was detected by reverse transcription-quantitative polymerase chain reaction. In addition, the effect of miR-30b on cell proliferation in RCC cells was also determined using MTT and Cell Counting Kit-8 assay analyses. Furthermore, the function of miR-30b in cell migration and invasion was determined by wound scratch and Transwell assays. Flow cytometry was also performed to quantify the effect of miR-30b on cell apoptosis. The results of the current study indicated that miR-30b was upregulated in RCC tissues from affected cell lines when compared with adjacent normal tissues and a normal kidney cell line, which is different to the downregulation of miR-30b as observed in other types of cancer. miR-30b is associated with RCC cell proliferation, invasion, migration and apoptosis, which indicated that miR-30b acts as an oncogene in RCC. To the best of our knowledge, the present study is the first to demonstrate the upregulation of miR-30b in RCC tissues and describe miR-30b as an oncogene in RCC in the regulation of cell proliferation, migration, invasion and apoptosis. Further studies will define the target gene of miR-30b in RCC and investigate the potential role of miR-30b as a biomarker for RCC. [ABSTRACT FROM AUTHOR]

miRNAs have been reported to be involved in multiple cellular processes and the tumorigenesis of various cancers. miR-15a-5p (also termed miR-15a) has previously been determined to be upregulated in renal cell carcinoma (RCC) by microarray profile. However, the expression and function of miR-15a-5p in RCC remain to be validated. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to detect the expression levels of miR-15a-5p in RCC tissues and cells. The expression level of miR-15a-5p was upregulated or downregulated by transfecting synthesized miR-15a-5p mimics or inhibitors. The MTT assay, CCK-8 assay, Transwell assay, wound healing assay, Hoechest 33342 staining and flow cytometry were conducted to investigate the role of miR-15a-5p in RCC. The results of the RT-qPCR demonstrated that miR-15a-5p was upregulated in RCC tissues and ACHN, 786-O and 769P RCC cells compared with paired normal tissues and HEK-293T cells. miR-15a-5p was observed to be associated with RCC cell proliferation, migration, invasion and apoptosis. The results demonstrated that miR-15a-5p may be important as a tumor promoter in RCC. To the best of our knowledge, the present study is the first to describe miR-15a-5p as a tumor promoter in RCC. Further research will be performed to investigate the underlying signaling pathway of miR-15a-5p and the potential role of miR-15a-5p as a biomarker for early detection, prognosis prediction and a therapeutic target of RCC. [ABSTRACT FROM AUTHOR]

Certain microRNAs (miRs) are implicated in the genesis and progression of various cancers by regulating multiple cellular processes, including apoptosis, proliferation and migration. The aim of the present study was to explore the functions of miR-196a in renal cell carcinoma (RCC). RCC and paired normal tissues we assessed for miR-196a expression by reverse-transcription quantitative PCR. Furthermore, the effects of miR-196a on renal cell proliferation, apoptosis and migration were determined using an MTT assay, flow cytometry and a scratch wound assay following restoration of miR-196a with synthetic mimics. miR-196a was found to be significantly downregulated in RCC tissues compared with that in normal tissues (P<0.05). In addition, miR-196a suppressed cell proliferation, apoptosis and migration of the 786-O and ACHN RCC cell lines. To the best of our knowledge, the present study was the first to report this tumor suppressor role of miR-196a in RCC. The results indicated that miR-196a may be a potential diagnostic biomarker for RCC and that transfection of miR-196a mimics may represent a novel treatment strategy for RCC. [ABSTRACT FROM AUTHOR]

Several studies have recently explored the role of microRNAs (miRNAs, miRs) in the tumorigenesis of various types of cancer. miRNAs have been reported to be involved in numerous cell processes, including cell apoptosis, proliferation and migration, thus suggesting that miRNAs may have an important role in cancer progression. Downregulation of miR-149-5p has been detected in RCC tissues by microarray profiling; however, its expression and function in RCC has yet to be elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction was performed to detect the expression levels of miR-149-5p in RCC tissues and paired normal tissues. In order to determine whether miR-149-5p was able to regulate cell proliferation, apoptosis or migration, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometric and wound healing assays were conducted. The results demonstrated that miR-149-5p was significantly downregulated in RCC tissues compared with in normal tissues (P<0.05). The restoration of miR-149-5p expression using synthetic mimics suppressed cell proliferation and migration, and promoted cell apoptosis. These results indicated that miR-149-5p may act as a tumor suppressor in RCC. The present study is the first, to the best of our knowledge, to identify miR-149-5p as a tumor suppressor in RCC. Future studies will be focused on the potential role of miR-149-5p as a biomarker for the early detection and prognostic prediction of RCC, and as a therapeutic target in RCC. In addition, further exploration regarding the pathways underlying the effects of miR-149-5p in RCC is required. [ABSTRACT FROM AUTHOR]

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]

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]

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]

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]

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 (miRNAs; miR) are a class of small non-coding RNA molecules, which are involved in the pathogenesis of human diseases through the negative regulation of gene expression. Previous studies have demonstrated that miR-509-3p is a novel miRNA associated with cell proliferation and migration in 786-O renal cell carcinoma (RCC) cells. However, the mechanism of action of miR-509-3p in RCC remains to be elucidated. The present study aimed to examine the functional role and mechanism of miR-509-3p in the development of RCC. The results demonstrated that the expression levels of miR-509-3p were downregulated in the 786-O and ACHN RCC cell lines compared with the normal tissues of 10 patients with RCC, as determined by reverse transcription-quantitative polymerase chain reaction. The mRNA expression levels of mitogen-activated protein kinase kinase kinase 8 (MAP3K8) were upregulated in the RCC cell lines. Functional investigations demonstrated that the overexpression of miR-509-3p inhibited the migration and proliferation of the RCC cells, as determined by wound scratch and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays. Luciferase reporter assays revealed that the overexpression of miR-509-3p reduced the transcriptional activity of MAP3K8. Furthermore, the present study demonstrated that the ectopic transfection of miR-509-3p led to a significant reduction in the mRNA and protein expression levels of MAP3K8 in the RCC cells. Finally, knockdown of MAP3K8 inhibited the migration and proliferation of the RCC cells. Therefore, the results of the present study demonstrated that the miR-509-3p RCC suppressor was a significant regulator of the MAP3K8 oncogene, suggesting that it may have a potential therapeutic role in the treatment 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]

MicroRNAs (miRNAs) are an important class of small, non-coding RNA molecules that regulate gene expression at the transcriptional or post-transcriptional level. They are involved in apoptosis, proliferation and migration and are known to have an important role in many types of cancer. Aberrant expression of miRNA-451a (miR-451a) has previously been reported in tumors, however its role in renal cell carcinoma (RCC) is currently unknown. The aim of the present study was to investigate the role of miR-451a in RCC. The expression of miR-451a was analyzed in 50 paired RCC and normal tissues by quantitative polymerase chain reaction. Furthermore, the effects of miR-451a on cell migration, proliferation and apoptosis were evaluated, using migration scratch, MTT and flow cytometric assays. The present study demonstrated that miR-451a was upregulated in RCC, as compared with paired normal tissues (P<0.05). Downregulation of miR-451a using a synthesized inhibitor, significantly suppressed cell migration and proliferation, and induced apoptosis of renal cancer cells in vitro, as compared with a negative control (P<0.05). In the present study, it was determined that miR-451a may have an important role as a tumor enhancer in RCC. These results imply that miR-451a may be a promising therapeutic target for the treatment of RCC. [ABSTRACT FROM AUTHOR]

microRNAs (miRNAs) are evolutionarily conserved, endogenous, small, noncoding RNA molecules of approximately 22 nucleotides in length that function as post-transcriptional gene regulators. Their aberrant expression may be involved in human diseases, including cancer. Although miRNA-184 (miR-184) has been reported in other tumors, its function in renal cell carcinoma (RCC) is still unknown. The aim of the present study was to investigate the role of miR-184 in RCC. The impacts of miR-184 on cell migration, proliferation and apoptosis were evaluated using migration scratch, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assay. Our studies revealed that miR-184 mimic significantly inhibits cell migration, suppresses cell proliferation and induces renal cancer cell apoptosis in vitro when compared with the negative control (P<0.05). In this study, it was observed that miR-184 played a significant role as a tumor suppressor in RCC. Therefore, miR-184 may be a promising therapeutic target for renal cancer treatment in the future. [ABSTRACT FROM AUTHOR]