MicroRNA-205 acts as a tumor suppressor in osteosarcoma via targeting RUNX2
Authors: Yihe Hu
Feng Long
Hongbo He
Jun Wan
Can Zhang
Journal: Oncology Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; gene expression; osteosarcoma; miR-205; regulatory mechanism
Affiliations: Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

Abstract:  MicroRNAs (miRs) are a class of small non-coding RNAs, and negatively regulate gene expression through directly binding to the 3'-untranslational region (UTR) of their target mRNA, which further leads to translational repression or mRNA degradation. Recently, various miRs have been implicated in the development and progression of osteosarcoma (OS). However, the underlying mechanism has not been fully uncovered. Our study aimed to reveal the exact role of miR-205 in OS, as well as the regulatory mechanism. In this study, we found that the expression of miR-205 was significantly reduced in a total of 34 OS tissue specimens compared to their matched adjacent normal tissues. Besides, it was also remarkably downregulated in OS cell lines (Saos-2, U2OS, SW1353, and MG63) compared to human osteoblast hFOB1.19 cells. Overexpression of miR-205 caused a significant decrease in the proliferation, migration and invasion of MG63 and U2OS cells. Runt-related transcription factor 2 (RUNX2) was further identified as a target gene of miR-205. Moreover, the mRNA and protein expression of RUNX2 was reduced after miR-205 overexpression, but increased after knockdown of miR-205 in MG63 and U2OS cells. Furthermore, overexpression of RUNX2 effectively reversed the suppressive effect of miR-205 on the proliferation, migration, and invasion of MG63 and U2OS cells. The RUNX2 level was significantly increased in OS tissues compared to their matched adjacent normal tissues, as well as in OS cell lines compared to hFOB1.19 cells. In addition, the RUNX2 level was reversely correlated with the miR-205 level in OS tissues. Taken together, our data demonstrate that miR-205 acts as a tumor suppressor in OS via directly targeting RUNX2. Therefore, we suggest that the miR-205/RUNX2 axis may serve as a potential target for the treatment of OS. 

Retracted: Yes

PubPeer comments:
 Fig 3 C D,  Transwell assay were performed to examine the migratory and invasive capacities of Saos-2 and U2OS cells transfected with miR-205 mimic or miR-negative control (NC) mimic , and Fig 7C D,  Transwell assay were performed to examine cell migration and invasion of MG63 or U2OS cells transfected with miR-205 mimic, or co-transfected with miR-205 mimic and RUNX2 plasmid .  Colored rectangles mark similar panels in Figs 2(C) and 4(C) of [Jiao et al (2016)] .  Also *[above]* Fig 4C from [Lai, Chen Li (2015)] .  a Transwell assay were performed to examine the cell proliferation of AGS cells transfected with miR-133a mimics, miR-133a inhibitor, or co-transfected with miR-133a mimics and FSCN1 plasmid. Control: AGS cells without any transfection. *[below]* Figs 3(B), 6(B) from [Shi et al (2015)] .  Transwell assay was performed to determine the invasive capacity of the Saos-2 and U-2 OS cells transfected with NC scramble miRNA or miR-204 mimics, respectively. Control, Saos-2 and U-2 OS cells without any transfection ...  Transwell assay was performed to determine the invasive capacity of the Saos-2 and U-2 OS cells transfected with Sirt1 siRNA or co-transfected with miR-204 mimics and the Sirt1 plasmid, respectively. Control, Saos-2 and U-2 OS cells without any transfection .  , 
 Retracted [7 June 2021] . ----------------------------------- Following the publication of this paper, it was drawn to the Editors attention by a concerned reader that certain of the cell Transwell assay data in the article (featured in Fig. 3C and D) were strikingly similar to data that appearing in different form in other articles by different authors at different research institutions, which were already under consideration for publication or had already been published elsewhere at the time of the present article s submission. Owing to the fact that the contentious data in the above article had already appeared in different form in other articles prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. ,