Abstract

MicroRNA (miR)-137 has been reported to be underexpressed and involved in various cell processes and to have antitumor effects in a range of tumors, but so far not in renal cell carcinoma (RCC). The aim of the present study was to investigate the clinical significance and role of miR-137 in RCC. The expression levels of miR-137 were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in 50 cases of paired RCC tissues and adjacent normal tissues, and in RCC cell lines. The role of miR-137 in the growth and survival of RCC cells was assessed with several in vitro approaches and in nude mice models. The results of the RT-qPCR showed that the miR-137 expression was downregulated in the RCC tissues and cell lines. The in vitro assay showed that ectopic expression of miR-137 robustly impaired RCC cell proliferation, migratory and invasive properties, and increased the induction of cell apoptosis properties. The in vivo assay demonstrated that enforced miR-137 suppressed tumor growth in xenograft nude mice models. In addition, miR-137 was indicated to inhibit the activation of phosphoinositide 3 kinase/protein kinase B signal pathway, which contributes to the inhibition of RCC growth. These findings indicate that miR-137 functions as tumor suppressor in RCC, suggesting that miR-137 may be a potential therapeutic target for RCC.

Highlights

  • Renal cell carcinoma (RCC) accounts for 3% of all adult malignancies and is the third most common urological cancer worldwide, with the highest mortality rate of RCC at >40% [1]

  • To determine whether miR‐137 expression is associated with RCC pathogenesis, the expression levels of miR‐137 were determined using reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR) analysis in 50 pairs of RCC and adjacent normal tissues

  • Chen et al showed that miR‐141 serves as a potential biomarker for discriminating RCC from normal tissues and a crucial suppressor of RCC cell proliferation and metastasis by modulating the EphA2/p‐FAK/p‐AKT/MMPs signaling cascade [19]

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Summary

Introduction

Renal cell carcinoma (RCC) accounts for 3% of all adult malignancies and is the third most common urological cancer worldwide, with the highest mortality rate of RCC at >40% [1]. 65,150 novel cases and 13,680 mortalities were estimated for 2013 in the USA [1]. Clear cell RCC (ccRCC) is the largest subtype of RCC and accounts for 70% of RCCs [2]. Despite the increasingly early detection of RCC and more frequent use of surgery, the mortality rate has not changed A better understanding of the mechanisms involved in the pathogenesis of RCC and more effective therapeutic approaches are urgently required

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