Open AccessMicroRNA-302a suppresses cell proliferation, migration and invasion in osteosarcoma by targeting ADAM9
Author(s) -
Yang Xiaoming,
Yan Cui,
Fuqiang Yang,
Chao Sun,
Xue-jian Gao
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.6975
Subject(s) - microrna , cancer research , gene knockdown , oncogene , cell growth , metastasis , downregulation and upregulation , biology , ectopic expression , osteosarcoma , cell , cell cycle , apoptosis , cell culture , cancer , gene , genetics
Osteosarcoma (OS) is the most frequent malignant primary bone tumor arising from primitive bone‑forming mesenchymal cells in children and adolescents. The dysregulation of microRNAs (miRNAs) has been reported in OS, and these aberrantly expressed miRNAs are involved in the initiation and progression of OS. The aim of the present study was to investigate the expression and functions of miRNA‑302a (miR‑302a) in OS and its underlying mechanism. It was found that the expression of miR‑302a was reduced in OS tissues and cell lines. The low expression of miR‑302a was significantly correlated with tumor‑node‑metastasis stage and metastasis. The ectopic overexpression of miR‑302a inhibited the proliferation, migration and invasion of OS cells. Bioinformatics analysis showed that a disintegrin and metalloproteinase 9 (ADAM9) was a potential target gene of miR‑302a. Subsequently, reverse transcription‑quantitative polymerase chain reaction and western blot analyses revealed that miR‑302a regulated the expression of ADAM9 at the post‑transcriptional level in OS cells. In addition, a luciferase reporter assay demonstrated that miR‑302a directly targeted the 3'untranslated region of ADAM9. In clinical OS tissues, the mRNA expression of ADAM9 was upregulated and inversely correlated with the expression of miR‑302a. In addition, the effects of ADAM9 knockdown on cell proliferation, migration and invasion were similar to those induced by the overexpression of miR‑302a in OS cells. These findings suggested that miR‑302a inhibited OS cell growth and metastasis by targeting ADAM9. miR‑302a may serve as a potential therapeutic target for patients with OS.