4.5 Article

miR-660-5p is associated with cell migration, invasion, proliferation and apoptosis in renal cell carcinoma

Journal

MOLECULAR MEDICINE REPORTS
Volume 17, Issue 1, Pages 2051-2060

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2017.8052

Keywords

microRNA; miR-660-5p; renal cell carcinoma; tumor suppressor

Funding

  1. National Natural Science Foundation of China [81101922]
  2. Science and Technology Development Fund Project of Shenzhen [JCYJ20150403091443329, JCYJ20170307111334308]
  3. fund of San-ming project of medicine in Shenzhen
  4. fund of Guangdong Key medical subject

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Renal cell carcinoma (RCC) is a common malignant tumor of the urinary system with poor prognosis. microRNAs (miRNAs) are a class of small, non-coding RNA molecules that serve important roles in biological and pathological processes in several types of human tumors. miRNA (miR)-660-5p is dysregulated in many human cancers; however, its role in renal cell carcinoma is currently unclear. In the present study, reverse transcription-quantitative polymerase chain reaction was performed to examine the expression levels of miR-660-5p in RCC tissues and paired normal adjacent tissues (NATs). To determine the function of miR-660-5p in RCC cells, wound-healing and Matrigel assays were performed to determine the effects of miR-660-5p on cell migration and invasion, respectively. MTT and Cell Counting kit-8 assays were performed to determine the effects of miR-660-5p on RCC cell proliferation. In addition, flow cytometric analysis was performed to validate the effects of miR-660-5p on apoptosis. The results indicated that miR-660-5p expression was downregulated in RCC tissues compared with NATs. Restoration of miR-660-5p expression using synthetic mimics may suppress cell migration, invasion and proliferation, and induce cell apoptosis, while using synthetic inhibitors may promote cell migration, invasion and proliferation, and suppress cell apoptosis. These results suggested that miR-660-5p may serve a tumor suppressive role in RCC tumorigenesis.

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