Xin Guan

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

MicroRNAs (miRs) are involved in diverse physiological and developmental processes at the post-transcriptional level in cells. Previous studies have demonstrated that miR-136-5p is involved in certain types of cancer. However, the function of miR-136-5p in renal cell carcinoma (RCC) remains to be fully elucidated. In present study, miR-136-5p expression levels were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and MTT assays, CCK-8 assays, Transwell assays, wound healing assays and flow cytometry were performed to investigate the function of miR-136-5p in RCC. RT-qPCR revealed that the expression of miR-136 was significantly lower in RCC tissues and cells compared with adjacent non-tumor tissues and cells in vitro. miR-136-5pwas also demonstrated to be associated with RCC cell proliferation, viability, migration, invasion and apoptosis. miR-136-5p may therefore function as a tumor suppressor in RCC. Further studies are required to elucidate the molecular mechanisms and signaling pathways underlying these functions of miR-136-5p, to investigate the potential function of miR-136-5p as a biomarker for the early detection and prognosis of RCC, and its potential as a therapeutic target for the treatment 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.

[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.

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.

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.

MicroRNA‑222‑3p promotes tumor cell migration and invasion and inhibits apoptosis, and is correlated with an unfavorable prognosis of patients with renal cell carcinoma

The aim of the present study was to investigate the role of microRNA (miR)‑222‑3p in renal cell carcinoma (RCC). The expression level of miR‑222‑3p was detected in RCC tissues and cell lines (ACHN, 786‑O, Caki‑1 and 769‑P) and was identified to be significantly upregulated compared with the level in adjacent normal renal tissues and HK‑2 cells. Further inxa0vitro experiments demonstrated that the over-expression of miR‑222‑3p promoted the migration and invasion, and attenuated the apoptosis of 786‑O cells, whereas the knockdown of miR‑222‑3p suppressed the migration and invasion and induced the apoptosis of 786‑O cells. Similar results were observed in the ACHN cell line in terms of migration, invasion and apoptosis. Furthermore, the expression level of miR‑222‑3p was measured in 42 RCC formaldehyde‑fixed paraffin‑embedded samples, and the association between the expression of miR‑222‑3p and the pathological characteristics and overall survival rate of patients with RCC was analyzed. The results demonstrated that patients with a higher expression of miR‑222‑3p had a significantly lower overall survival rate, compared with those with a lower expression of miR‑222‑3p [hazard ratio (HR)=5.120; P=0.036]. Multivariate analysis identified that patients with a higher expression of miR‑222‑3p retained the statistically significant decrease in overall survival rate compared with patients with a lower expression of miR‑222‑3p (HR=5.636; P=0.030). Furthermore, Kaplan‑Meier survival curves indicated that patients with higher miR‑222‑3p had significantly lower overall survival rates compared with patients with lower miR‑222‑3p (P=0.020). Taken together, these results suggested that miR‑222‑3p serves as an onco‑miR in RCC and may be a potential prognostic biomarker and therapeutic target in patients with RCC.

[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.

miR-216a-5p acts as an oncogene in renal cell carcinoma

MiR-216a-5p has been acknowledged as an oncogene and is known to be involved in the progression and metastasis of numerous cancer subtypes. However, the potential role of miR-216a-5p in renal cell carcinoma (RCC) remains to be elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction was performed to detect the expression levels of miR-216a-5p in RCC tissues. Cell counting kit-8, MTT, wound scratch, Transwell and flow cytometric assays were performed to establish the biological functions of miR-216a-5p in RCC. Functional experiments demonstrated that the expression of miR-216a-5p was upregulated in RCC (P<0.05) and miR-216a-5p mimics promoted cellular proliferation, viability and motility, and suppressed apoptosis. Conversely, miR-216a-5p inhibitor suppressed cellular proliferation, viability, motility and induced apoptosis. Based on these findings, it was concluded that miR-216a-5p may function as an oncogene in RCC. MiR-216a-5p target genes need to be explored and the potential of miR-216a-5p to be used as a diagnostic or a prognostic biomarker for RCC needs to be validated by future research.