Jing Quan

Overexpression of long non-coding RNA differentiation antagonizing non-protein coding RNA inhibits the proliferation, migration and invasion and promotes apoptosis of renal cell carcinoma

Renal cell carcinoma (RCC) is the third most common cancer in the urological system; however, the pathogenesis remains unknown. Accumulating evidence has demonstrated that long non‑coding RNAs are dysregulated in various tumors and serves an important role in tumorigenesis and development. In the present study, expression of lncRNA differentiation antagonizing non‑protein coding RNA (DANCR) in 24 paired RCC and adjacent normal tissues was detected by reverse transcription‑quantitative polymerase chain reaction. The results revealed that DANCR is downregulated in RCC tissues compared with adjacent normal tissues. Subsequent study revealed that overexpression of lncRNA DANCR by transfection of pcDNA3.1‑DANCR could suppress 786‑O and ACHN (RCC cell) proliferation, migration and invasion, and induce apoptosis compared with cells transfected with the pcDNA3.1 vector. The results revealed that DANCR functions as a tumor suppressor in RCC. In conclusion, the present study, to the best of our knowledge, was the first to reveal DANCR as a tumor suppressor. The results implicate DANCR as a potential biomarker of RCC, and further study will be focused on the clinical significance and signaling pathways of DANCR.

Identification of lncRNA EGOT 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. Long non‑coding RNA (lncRNA) is a class of RNA which serves important roles in multiple cellular processes and tumorigenesis. In the present study, the expression and function of lncRNA eosinophil granule ontogeny transcript (EGOT) were examined in RCC. In 24 paired tissues (RCC tissues and adjacent normal tissues) the results of reverse transcription‑quantitative polymerase chain reaction analysis revealed that EGOT was downregulated in 22 RCC tissues compared with paired tissues. Upregulation of lncRNA EGOT by transfection of 786‑O and ACHN RCC cells with pcDNA3.1‑EGOT suppressed cell proliferation, migration and invasion, and induced RCC cell apoptosis. The results demonstrated that EGOT may serve as a tumor suppressor in RCC and may be a potential prognostic biomarker of 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.

MicroRNA‑191‑5p exerts a tumor suppressive role in renal cell carcinoma

Renal cell carcinoma (RCC) is a common tumor of the urinary system. Previously, miR-191-5p has been reported to be associated with various types of cancer; however, its specific functions in RCC have not been investigated to date. In the present study, the expression of miR-191-5p in the 786-O and ACHN cell lines was detected in vitro by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results of RT-qPCR revealed that miR-191-5p was significantly downregulated in the two cell lines compared with the 293T cell line. miR-191-5p was also significantly downregulated in RCC tissue compared with paired normal tissue. In addition, the effects of miR-191-5p on cell proliferation, migration, invasion and apoptosis were examined by CCK-8, MTT, wound scratch, Transwell and flow cytometry assays. Downregulation of miR-191-5p was observed to promote cell proliferation, migration and invasion, as well as to repress the cell apoptosis of 786-O and ACHN cells. Therefore, the current study suggests that miR-191-5p functions as a tumor suppressor in RCC. Further studies are required to uncover the underlying signaling pathway of miR-191-5p and its potential role as a biomarker for early detection and prognosis prediction, and as a therapeutic target of RCC.

microRNA‑572 functions as an oncogene and a potential biomarker for renal cell carcinoma prognosis

Renal cell carcinoma (RCC) is the third most common urological malignancy in the USA and represents 2‑3% of all adult malignancies. Furthermore, the incidence of RCC has been progressively increasing over recent years. Although the morbidity of treatment has decreased with the use of multidisciplinary synthetic therapy, the prognosis of terminal cancer remains poor, with a 5‑year survival rate of 5‑10%. MicroRNAs (miRs) have been correlated with the regulation of 30‑60% of the protein-coding genes and act as oncogenes or anti‑oncogenes in RCC. Considering this research, miRNAs are likely to be the biomarkers for tumor diagnosis, prognosis and the targets for RCC management. In the present study, 42 formalin‑fixed paraffin‑embedded RCC samples were used. The expression of miR‑572 and the role of miR‑572 in RCC cell proliferation, migration and apoptosis was determined by performing reverse transcription‑quantitative polymerase chain reaction analysis, wound scratch assays, cell proliferation assays, Transwell assays and flow cytometry assays, respectively. Further experiments were conducted to clarify the correlation between miR‑572 expression and clinicopathological variables or overall survival. Furthermore, the expression levels of miR‑572 were evaluated for the prognosis value of patients with RCC. Upregulation of miR‑572 was observed in RCC tissues and RCC cell lines. miR‑572 promoted 786‑O and ACHN cell proliferation and mobility and inhibited early apoptosis. In Cox proportional hazard regression analyses, results of the univariate and multivariate analysis indicated that the patients with low miR‑572 expression had a significantly longer overall survival compared with the patients with high miR‑572 expression (univariate analysis, P=0.037; multivariate analysis, P=0.034). Results of the Kaplan‑Meier survival curves revealed that the patients with downregulated miR‑572 have a significantly longer overall survival compared with the patients with highly expressed miR‑572 (P=0.019). To conclude, the results of the present study suggest that tumor oncogene miR‑572 is a potential biomarker for the diagnosis, treatment and prognosis 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] microRNA‑181a‑5p functions as an oncogene in renal cell carcinoma

Subsequently to the publication of the article, the authors have recognized a need to correct some of its content in order to clarify the accuracy of the articles information. First, Dr Yongqing Lai should have been included as the joint corresponding author for this paper. Therefore, the information in the correspondence box should have been as follows (changes are indicated in bold): Correspondence to: Professor Liangchao Ni or Dr Yongqing Lai, Department of Urology, Peking University Shenzhen Hospital, 1120 Lianhua Road, Shenzhen, Guangdongxa0518036, P.R.xa0China. E‑mail: lncord@163.com, E‑mail: yqlord@163.com. Secondly, the printed version of Fig.xa05 featured an incorrect alignment of the scratch wound scratch assay results showing the migratory ability of the 786‑O cells (the lower panel). The corrected version of Fig.xa05 is featured opposite. These errors did not have an impact on the overall meaning of the paper, or on the reported conclusions of this study. We regret that these errors were not incorporated into the printed version of the paper, and apologize to the readership for the inconvenience caused. [the original article was published in the Molecular Medicine Reports 17: 8510‑8517, 2018; DOI: 10.3892/mmr.2018.8899].

microRNA‑181a‑5p functions as an oncogene in renal cell carcinoma

Renal cell carcinoma (RCC) is one of the most common urinary tumors. Previous studies have demonstrated that microRNA (miR)‑181a‑5p has an important role in numerous types of cancer. However, the function of miR‑181a‑5p in RCC remains unknown. In the present study, the expression levels of miR‑181a‑5p in RCC tissues and cell lines were investigated using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis. The results of the RT‑qPCR analyses suggested that the expression of miR‑181a‑5p was upregulated in RCC tissues and cells lines compared with adjacent normal renal tissues and normal renal cell lines. Furthermore, the effect of miR‑181a‑5p on cell proliferation, migration, invasion and apoptosis was investigated in the present study. Overexpression of miR‑181a‑5p was revealed to suppress the apoptosis of 786‑O and ACHN cells, in addition to enhancing the proliferation, migration and invasion abilities of 786‑O and ACHN cells inxa0vitro, thus suggesting that miR‑181a‑5p may function as an oncogene in RCC. However, further studies are required to investigate the underlying mechanism of miR‑181a‑5p and its potential role as a biomarker for early detection and prognosis, in addition to as a therapeutic target in RCC.

Suppressing cell growth and inducing apoptosis by inhibiting miR‑23a‑5p in human bladder cancer

MicroRNAs (miRNAs) are a class of non‑coding RNAs, which are important in the initiation and progression of cancer. miRNA‑23a‑5p (miR‑23a‑5p) is a novel miRNA, which promotes cell growth and survival in several types of cancer. The aim of the present study was to investigate the expression and functional significance of miR‑23a‑5p in bladder cancer. Microchip assays have shown that miR‑23a‑5p is significantly upregulated in human bladder cancer. In the present study, it was found that miR‑23a‑5p was upregulated in bladder cancer tissues, compared with paired normal urothelial tissues by reverse transcription‑quantitative polymerase chain reaction. The impact of miR‑23a‑5p on cell proliferation, cell migration and apoptosis was determined by a 3‑(4,5‑dimethylthi‑azol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assay, wound scratch assay and flow cytometry. The inhibition of cell proliferation and induction of apoptosis were also observed in miR‑23a‑5p inhibitor‑transfected T24 and SW780 human bladder cancer cells. These data suggested that miR‑23a‑5p has an oncogenic role and may be a therapeutic target for bladder cancer.

MiR-302b regulates cell functions and acts as a potential biomarker to predict recurrence in bladder cancer

Background: Bladder cancer is the most common urogenital tumor with substantial morbidity, high recurrence rate and mortality. miRNAs, a class of endogenous noncoding RNA, were found to involve in the genesis, maintenance and metastasis of cancer. Genomic profiling revealed that miR‐302b is down‐regulated in bladder cancer while its functions in bladder cancer remain to be ascertained. Methods: Cell functional assays including wound healing assay, CCK‐8 assay, Transwell assay and flow cytometry assay were performed to clarify the functions of miR‐302b expression in cell proliferation, migration, invasion and apoptosis in BC. Furthermore, RT‐qPCR was performed to study the expression of miR‐302b in bladder cancer tissues and the prognostic value of altered miR‐302b expression with 48 formalin‐fixed paraffin‐embedded bladder urothelial carcinoma samples. Results: The results of RT‐qPCR demonstrated that expression level of miR‐302b was significantly reduced in bladder cancer tissues and cell lines. The cells after transfected with miR‐302b mimic showed lower mobility, lower proliferation and increased apoptosis, while opposite results were obtained after inhibiting the expression of miR‐302b. The prognosis analysis demonstrated that the patients with low expression of miR‐302b experienced high risks of recurrence. Conclusions: The results of our study demonstrate that miR‐302b regulates cell functions and acts as a potential biomarker to predict recurrence in bladder cancer.