MicroRNA-137 acts as a tumor suppressor in osteosarcoma by targeting enhancer of zeste homolog 2
Authors: Hui Li
Yanfei Xiong
Xing Liu
Qing Wu
Qiong Feng
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: enhancer of zeste homolog 2; microRNA-137; osteosarcoma; tumor suppressor.
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.

Abstract:  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&lt;0.01). Moreover, it was observed that low miR-137 expression levels were significantly associated with lung metastasis and advanced TMN stage (P&lt;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&lt;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&lt;0.01). EZH2 was significantly downregulated following miR-137 overexpression (P&lt;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&lt;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. 

Retracted: Yes

PubPeer comments:
 Fig 7A.  Western blotting was performed to examine levels of EZH2 protein. ![file] Fig 7 of [Dai et al (2016)] . ![file] Fig 6B from [Zhou et al (2017)] . Figs 7A,B, 9B from [Liu et al (2017)] . Figs 3B, 4B from [Dang et al (2017)] . Fig 4A from [Jiang et al (2017)] . ![file] , 
 Figs 2C, 3C, 7C. Transwell assays. ![file] Could the authors comment on the shared panels with Figs 5C, 6E of [Zhou et al (2018)] ? ![file] And Figs 5C,D and 7A,B of [Li et al (2018)] ? ![file] ------------------------------------------------------------------------------ The repeated motifs in Fig 1C also call out for an explanation. ![file] , 
 Retracted [12 August 2021] . ----------------------------------- Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that the western blotting data shown in Fig. 7A, were strikingly similar to data appearing in different form in other articles by different authors. Furthermore, there were possible anomalies associated with the Transwell cell migration assay data shown in Fig. 1C. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to *Experimental and Therapeutic Medicine*, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused , 
 #3 u201cpossible anomaliesu201d ,