MicroRNA-204 inhibits proliferation, migration, invasion and epithelial-mesenchymal transition in osteosarcoma cells via targeting Sirtuin 1
Authors: Jun Zhou
Gang Yin
Jianjun Huang
Xiaodan Fu
Yimin Li
Ying Liu
Ying Shi
Jifang Wen
Journal: Oncology Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; miR-204; osteosarcoma; tumor suppressor; proliferation
Affiliations: Department of Pathology, School of Basic Medicine, Central South University, Changsha, Hunan 410013, P.R. China., The Second Department of Orthopedics, The First Affiliated Hospital of Jishou University, Jishou, Hunan 416000, P.R. China.

Abstract:  MicroRNAs (miRs) play crucial roles in tumorigenesis by directly suppressing the protein expression levels of their target genes. miR-204 has been suggested to act as a tumor suppressor in several types of human cancer. However, the exact role of miR-204 in osteosarcoma (OS) remains undetermined. In the present study, we aimed to investigate the effects of miR-204 on OS cell proliferation, migration and invasion, as well as the underlying molecular mechanisms. We found that the expression of miR-204 was frequently downregulated in four OS cell lines compared to the level in normal human osteoblast cells. Moreover, overexpression of miR-204 significantly inhibited the proliferation, migration and invasion of OS cells. Based on bioinformatics prediction and a luciferase reporter assay, we identified Sirtuin 1 (Sirt1) as a direct target gene of miR-204 in OS Saso-2 cells. Moreover, the protein expression of Sirt1 was negatively mediated by miR-204 in the OS cells. siRNA-mediated knockdown of Sirt1 also inhibited the proliferation, migration and invasion of the OS cells. Moreover, overexpression of Sirt1 reversed the inhibitory effect of miR-204 overexpression on the proliferation, migration and invasion of the OS cells. In addition, after miR-204 overexpression or Sirt1 knockdown in OS cells, the expression of E-cadherin was increased, while the N-cadherin protein level was reduced. Based on these findings, we suggest that miR-204 inhibits the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of OS cells by directly targeting Sirt1. 

Retracted: Yes

PubPeer comments:
 *[below]* Figs 3(B), 6(B).  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 . *[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. ![file] Several panels are shared across two otherwise-unrelated papers. How to explain the coincidence? , 
 Now with some additional mark-up: ![file] Highlighting similarity to panels of Figs 2(C) and 4(C) of [Jiao et al (2016)] . ![file] , 
 *[left]* Fig 7.  Western blot assay was performed to determine the protein levels of E-cadherin and N-cadherin in Saos-2 cells transfected with miR-204 mimics or Sirt1 siRNA, respectively . *[right]* Fig 3B from [Xiao, Liu Zhou (2016)] .  western blotting assays were performed to examine the ... protein levels of DLCu20111 in H1229 cells transfected with DLCu20111 plasmid or blank vector . Unexpected similarity after 180-deg flip. ![file] , 
 Retracted [31 May 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 Figs. 3B and 6B) were strikingly similar to data that appearing in different form in another article by different authors at different research institutions, which 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 another article prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors did not reply to indicate whether or not they agreed with the retraction of the paper. The Editor apologizes to the readership for any inconvenience caused. ---------------------------------------- Background [here] . ,