Yulin Lai

Upregulated microRNA-16 as an oncogene in renal cell carcinoma

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.

MicroRNA‑106b functions as an oncogene in renal cell carcinoma by affecting cell proliferation, migration and apoptosis

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.

Oncogenic miR-23a-5p is associated with cellular function in RCC

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.

Oncogenic miR‑425‑5p is associated with cellular migration, proliferation and apoptosis in renal cell carcinoma

An increasing number of studies have demonstrated the function of microRNAs (miRNAs) in the initiation and development of various types of cancer. Among them, miR-425-5p is proven to serve an important function in several types of cancer, including gastric, cervical cancer, and hepatocellular carcinoma. However, the function of miR-425-5p in renal cell carcinoma (RCC) remains unclear. In the present study, it was demonstrated that the expression level of miR-425-5p was upregulated in RCC tissues and cell lines compared with normal tissues and cell lines (P<0.05). Additionally, Cell Counting kit-8 and MTT assays were employed to assess cell viability and proliferation, whereas wound healing and Transwell assays were employed to examine migration and invasion. The results demonstrated that upregulation of miR-425-5p promoted cell viability and the invasion and migration of ACHN and 786O cells (P<0.05). Flow cytometric analysis confirmed that upregulation of miR-425-5p inhibited apoptosis of ACHN and 786O cells (P<0.05). Downregulation of miR-425-5p inhibited the viability and invasion and migration of ACHN and 786O cells (P<0.05). In the present study, upregulation of miR-425-5p inhibited apoptosis of ACHN and 786O cells whereas no differences in early apoptotic rate were observed between the inhibitor and inhibitor NC groups for 786O and ACHN cells. These results indicate that miR-425-5p may act as an oncogene in RCC.

[Corrigendum] Adrenal collision tumor (parachordoma and ganglioneuroma): A case report

[This corrects the article DOI: 10.3892/mco.2018.1610.].

Adrenal collision tumor (parachordoma and ganglioneuroma): A case report

Adrenal collision tumors (ACTs) are distinct tumors that occur simultaneously in the same adrenal gland and are very rare. We herein report the case of a 56-year-old woman who was admitted to the hospital for medical imaging. The findings of the physical and laboratory examinations, including endocrine function, were unremarkable. Contrast-enhanced computed tomography of the abdomen revealed a 28×20×33-mm mass in the left adrenal medial limb, for which a laparoscopic surgery was performed. Postoperative pathological examination revealed two distinct tumors, namely a parachordoma and a ganglioneuroma. To the best of our knowledge, and following a thorough literature search, this is the first report of coexisting parachordoma and ganglioneuroma in the same adrenal gland.

Oncogene miR-154-5p regulates cellular function and acts as a molecular marker with poor prognosis in renal cell carcinoma

Aims: In adult population, the renal cell carcinoma (RCC) is one of the most common urological malignancies. It is meaningful to research for the molecular markers which are involved in the occurrence and development of RCC. Therefore, we concentrate on illuminating the role of microRNA‐154‐5p in progression of RCC and explore its prognostic values. Main methods: The real‐time quantitative polymerase chain reaction (RT‐qPCR) was applied to determine expression level of miR‐154‐5p in tissues. Afterwards, the transfected cell lines ACHN and 786‐O were used for the CCK‐8 assay, MTT assay, wound healing assay, transwell assay and flow cytometric assay to explore the role of miR‐154‐5p in regulating cellular function. In addition, formalin‐fixed paraffin‐embedded (FFPE) renal cancer samples were used for detecting the relationship between expression level of miR‐154‐5p and clinical information. Furthermore, univariate and multivariate Cox proportional‐hazards regression analyses, and the Kaplan‐Meier survival curves were performed to evaluate the prognostic value of miR‐154‐5p in RCC. Key findings: The RT‐qPCR indicated that miR‐154‐5p is up‐regulated in RCC pathologic specimens and cell lines. Results of study also demonstrated that upregulation of miR‐154‐5p reduced cell apoptosis and promoted cell proliferation, viability, migration as well as invasion in RCC cells. The prognosis analyses indicated that the expression level of miR‐154‐5p is associated with the prognosis of renal cancer, and the overall survival of patients with low expression is longer. Significance: The present study revealed that the oncogene miR‐154‐5p regulates cellular function and acts as a molecular marker with poor prognosis in renal cell carcinoma.

[Corrigendum] miR‑199b‑5p serves as a tumor suppressor in renal cell carcinoma

[This corrects the article DOI: 10.3892/etm.2018.6151.].

miR‑199b‑5p serves as a tumor suppressor in renal cell carcinoma

MicroRNA (miR)-199b-5p has been reported to have a critical role in various types of malignancy. However, the exact function miR-199b-5p in renal cancer remains to be fully elucidated. The present study aimed to detect the expression levels of miR-199b-5p in renal cell carcinoma (RCC) tissues and RCC cell lines, and investigated the effect of miR-199b-5p in vitro with Cell Counting Kit-8, MTT, scratch wound, Transwell and flow cytometric assays. The results demonstrated that the expression levels of miR-199b-5p were significantly downregulated in RCC tissues and cell lines compared with those in paired adjacent normal renal tissues and a reference cell line, respectively. Downregulation of miR-199b-5p by transfection with a synthetic inhibitor promoted cellular proliferation and migration, while reducing the apoptotic rate, indicating that miR-199b-5p may serve as a tumor suppressor in RCC. Further study is required to identify target genes of miR-199b-5p to elucidate the mechanisms underlying the role of miR-199b-5p in the occurrence and development of RCC.

Oncogenic miR-663a is associated with cellular function and poor prognosis in renal cell carcinoma

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.