Jiaju Liu

Tumor suppressive miR-196a is associated with cellular migration, proliferation and apoptosis in renal cell carcinoma.

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.

MicroRNA-20b-5p functions as a tumor suppressor in renal cell carcinoma by regulating cellular proliferation, migration and apoptosis

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.

miR-125b is associated with renal cell carcinoma cell migration, invasion and apoptosis

MicroRNA (miR)-125b has been identified as deregulated in a number of types of cancer. Previous studies have detected the expression of miR-125b in clear cell renal cell carcinoma (ccRCC) tissues by in situ hybridization and revealed that miR-125b was upregulated in ccRCC tissues, and was associated with recurrence and survival of patients with ccRCC. However, the function of miR-125b in RCC remains unclear. Thus, the expression of miR-125b was detected with quantitative polymerase chain reaction (qPCR) in 24 paired RCC and adjacent normal tissues. The result of qPCR showed that miR-125b was upregulated in RCC tissues. Furthermore, the function of miR-125b in RCC (786-O and ACHN) cells was detected by transfecting miR-125 mimic or inhibitor to upregulate or downregulate miR-125b expression. Cell proliferation assays (MTT and Cell Counting Kit-8), cell mobility assays (cell scratch and Transwell assay) and a cell apoptotic assay (flow cytometry assay) were performed to assess the function of miR-125b on RCC cells. Results from the assays demonstrated that overexpression of miR-125b could promote cell migration and invasion, and reduce the cell apoptotic rate. It was also revealed that downregulation of miR-125b could reduce cell migration and invasion, and induce cell apoptosis. However, the results of the cell proliferation assay revealed that miR-125b had no significant effect on cell proliferation. Not only could miR-125b predict recurrence and survival of ccRCC; the present study revealed that miR-125b could regulate RCC cell migration, invasion and apoptosis. Additional studies are required to determine the mechanism of miR-125b in RCC cells and define the target genes of miR-125b in RCC.

Identification of miR‑195‑3p as an oncogene in RCC

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.

miR‑514a‑3p functions as a tumor suppressor in renal cell carcinoma

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 significantly 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.

Multilocular cystic renal cell carcinoma: A case report and review of the literature

Multilocular cystic renal cell carcinoma (MCRCC), which exhibits low-stage and low-grade characteristics, is a special type of RCC. MCRCC is extremely rare and generally develops at ages >50 years. We herein report a case of MCRCC in a 28-year-old man, which, to the best of our knowledge, is the youngest case reported worldwide to date. The patient presented with irritative bladder symptoms for 1 year. Dynamic enhanced computed tomography (CT) imaging revealed a mass with inhomogeneous enhancement in the left kidney, with a rich blood supply. B-ultrasonography also revealed a renal protruding mass. As the mass was highly suspicious to be a malignant tumor, laparoscopic radical nephrectomy was performed and MCRCC was definitively diagnosed by pathological examination. The patient has been regularly followed up for 6 months, without complications or disease recurrence.

MicroRNA‑24‑2 is associated with cell proliferation, invasion, migration and apoptosis in renal cell carcinoma

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.

Identification of miR‑130b as an oncogene in renal cell carcinoma.

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.