Renal cell carcinoma (RCC), a heterogeneous type of cancer originating from the nephron, occupies approximately 3.9% of new carcinomas, with an increasing incidence in the past two decades. The most common subtype of renal cell carcinoma is clear cell RCC (ccRCC). Though surgery and other treatments are applied to RCC, it has the highest recurrence rate and mortality rate among the genitourinary cancers. As the study progressed, miRNAs are found to be the biomarkers for tumor diagnosis, prognosis and the targets for tumor management.In present study, RT-qPCR, wound scratch assay, cell proliferation assay, transwell assay and flow cytometry assay were performed to ascertain miR-566 expression level and its proliferation, migration and apoptosis in RCC. Moreover, we analyzed the relation between miR-566 expression and clinicopathological variables or overall survival from the 42 formalin-fixed paraffin-embedded (FFPE) renal cancer samples. We further evaluate prognostic values of miR-566 expression.miR-566 is up-regulated in RCC tissue samples and renal carcinoma cell lines. miR-566 promotes cell proliferation, mobility and inhibits cell apoptosis in 786-O and ACHN cell lines. Cox proportional hazard regression analysis indicates that low expression of miR-566 patients have a remarkable longer overall survival in the univariate and multivariate analysis. The Kaplan-Meier survival curves show that the low expression of miR-566 patients have a remarkable longer overall survival.The results of the current study demonstrate that oncogene miR-566 is a potential biomarker not only for diagnosis but also for prognosis for RCC.
Following the publication of the above article and a corrigendum (10.3892/etm.2018.6333) that was concerned with changes in the authorship and affiliation details on the paper, an interested reader has drawn to the authors’ attention that, in Fig. 5A on p. 441, the ‘ACHN/cell invasion/miR‑199b‑5p inhibitor’ and ‘ACHN/cell invasion/NCin’ data panels appeared to show an overlapping section of data, such that they were derived from the same original source when they were intended to show the results from differently performed experiments. The authors have re‑examined their data, and realize that the ‘ACHN/cell invasion/NCin’ data panel was inadvertently selected incorrectly. The corrected version of Fig. 5, now containing the correct data for the ‘ACHN/cell invasion/NCin’ experiment, is shown on the next page. Note that the error made during the compilation of this figure did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of Experimental and Therapeutic Medicine for offering them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [Experimental and Therapeutic Medicine 16: 436‑444, 2018; DOI: 10.3892/etm.2018.6151]
OBJECTIVE: Renal cell carcinoma (RCC) is one of the most common genitourinary cancers, and advanced RCC usually leads to poor prognosis. Therefore, identifying novel biomarkers for predicting the progression and prognosis of RCC is essential. The present study aims to evaluate the clinical value of miR-183-5p in RCC development and prognosis after surgery. MATERIALS AND METHODS: We enrolled a total of 284 patients who received partial or radical nephrectomy from April 2003 to May 2013 at a single institution. The clinical and pathological characteristics of the patients were collected, including age, gender, tumor size, tumor stage, as well as follow-up information. The expression levels of miR-183-5p of all the patients were calculated from FFPE specimens. Cox regression analyses were performed to approve the effect of miR-183-5p expression on patient survival. Kaplan-Meier method was used to analyze the patient survival curves. RESULTS: After controlling for gender, age, tumor size and tumor stage in the multivariate analysis, we found that high expression of miR-183-5p was independently associated lower overall survival (HR = 0.550, 95% CI = 0.364–0.832, p= 0.005). The Kaplan-Meier analysis also showed that patients with high expression of miR-183-5p had a significantly poor prognosis (p= 0.006). These results was verified by analyzing the data of 506 cases from The Cancer Genome Atlas database (TCGA). CONCLUSION: Our results indicated that the high miR-183-5p expression is an independent factor for predicting RCC's worse prognosis.
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.
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 article’s information. First, Dr Yongqing Lai should have been included as the joint corresponding author for this paper. Therefore, the information in the correspondence box (also including his email address) should have been as follows (changes are indicated in bold): Correspondence to: Professor Liangchao Ni and Dr Yongqing Tai, Department of Urology, Peking University Shenzhen Hospital, 1120 Lianhua Road, Shenzhen, Guangdong 518036, P.R. China E‑mail: lncord@163.com E‑mail: yqlord@163.com Secondly, the authors wished to add two new authors (Canbin Lin and Hang Li) to the paper. Note that all the existing authors agree to the addition of these new authors; therefore, the revised author list is as appears above (with the newly added authors appearing third and fourth in the author list), and the affiliations should have appeared as follows: YULIN LAI1,2,5*, JING QUAN1,3,5*, CANBIN LIN1,4,5, HANG LI1,5, JIA HU1,2, PEIJIE CHEN1,4,5, JINLING XU1,5, XIN GUAN1,5, WEIJIE XU1,5, YONGQING LAI1,5 and LIANGCHAO NI1,5 1Department of Urology, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036; 2Graduate School, Guangzhou Medical University, Guangzhou, Guangdong 511436; 3Graduate School, Anhui Medical University, Anhui Hefei 230032; 4Graduate School, Shantou University Medical College, Shantou, Guangdong 515041; 5The Guangdong and Shenzhen Key Laboratory of Male Reproductive Medicine and Genetics, Peking University Shenzhen Hospital, Institute of Urology of Shenzhen PKU‑HKUST Medical Center, Shenzhen, Guangdong 518036, P.R. China *Contributed equally Lastly, the authors inadvertently omitted the reference number for the funding received from the ‘San‑ming’ Project of Medicine in Shenzhen: The ref. no. should have appeared as SZSM201612066. The authors regret that these errors and omissions were not corrected prior to the publication of the paper, and apologize to the readership for the inconvenience caused. [the original article was published in Experimental and Therapeutic Medicine Med 16: 436‑444, 2018; DOI: 10.3892/etm.2018.6151]
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