MicroRNA-137 acts as a tumor suppressor in osteosarcoma by targeting enhancer of zeste homolog 2
- Qiong Feng
- Qing Wu
- Xing Liu
- Yanfei Xiong
- Hui Li
Affiliations: Nursing School, Nanchang University, Nanchang, Jiangxi 330006, P.R. China, Department of Orthopedics, Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China, Department of Orthopedics, Jing An Hospital, Yichun, Jiangxi 330600, P.R. China, Department of Immunology and Microbiology, Medical School of Jishou University, Jishou, Hunan 416000, P.R. China
- Published online on: May 5, 2017 https://doi.org/10.3892/etm.2017.4435
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MicroRNA (miR) are short non‑coding RNA that bind to the 3'‑untranslational region of their target genes, inhibiting translation and causing mRNA degradation. miR deregulation has been implicated in human cancer; however, the detailed regulatory mechanism of miR‑137 in osteosarcoma (OS) remains largely unknown. In the present study, miR‑137 and enhancer of zeste homologue 2 (EZH2) mRNA and protein expression levels were analyzed using reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. MTT and transwell assays were performed to evaluate cell viability and invasion capacities and a luciferase reporter gene assay was used to determine the targeting relationship. The results of the current study indicated that miR‑137 expression was significantly downregulated in OS tissues and cell lines (P<0.01). Moreover, it was observed that low miR‑137 expression levels were significantly associated with lung metastasis and advanced TMN stage (P<0.05), but not associated with age, gender, tumor size, location, serum lactate dehydrogenase or serum alkaline phosphatase. Increasing levels of miR‑137 significantly inhibited U2OS cell viability and invasion (P<0.01). By contrast, knockdown of miR‑137 markedly increased U2OS cell viability and invasion. EZH2 was identified as a direct target gene of miR‑137 in U2OS cells by luciferase reporter assay and EZH2 expression was found to be significantly increased in OS tissues and cell lines (P<0.01). EZH2 was significantly downregulated following miR‑137 overexpression (P<0.01), and was upregulated following miR‑137 knockdown in U2OS cells. Furthermore, EZH2 overexpression significantly attenuated the suppressive effects of miR‑137 on U2OS cell viability and invasion (P<0.01), suggesting that miR‑137 inhibits the viability and invasion of OS cells by targeting EZH2. Therefore, the results of the current study suggest that the miR‑137/EZH2 axis may be a potential target for novel potential therapeutic strategies to treat OS.