RETRACTED: MicroRNA-137 acts as a tumor suppressor in osteosarcoma by targeting enhancer of zeste homolog 2 (Retracted article. See vol. 22, 2021)

被引:11
作者
Feng, Qiong [1 ]
Wu, Qing [2 ]
Liu, Xing [2 ]
Xiong, Yanfei [3 ]
Li, Hui [4 ]
机构
[1] Nanchang Univ, Nursing Sch, Nanchang 330006, Jiangxi, Peoples R China
[2] Nanchang Univ, Affiliated Hosp 2, Dept Orthoped, 1 Minde Rd, Nanchang 330006, Jiangxi, Peoples R China
[3] Jing An Hosp, Dept Orthoped, Yichun 330600, Jiangxi, Peoples R China
[4] Jishou Univ, Med Sch, Dept Immunol & Microbiol, Jishou 416000, Hunan, Peoples R China
关键词
osteosarcoma; microRNA-137; enhancer of zeste homolog 2; tumor suppressor; REGULATES CELL-PROLIFERATION; INHIBITS PROLIFERATION; INVASION; EZH2; DIFFERENTIATION; EXPRESSION; CARCINOMA; MIGRATION; GROWTH; CANCER;
D O I
10.3892/etm.2017.4435
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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.
引用
收藏
页码:3167 / 3174
页数:8
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