miR-150 is downregulated in osteosarcoma and suppresses cell proliferation, migration and invasion by targeting ROCK1
Authors: Hong-Wei Qiu
Chang-Hui Li
Chuan-Li Zhou
Chao Qi
Xia Zhao
Teng-Bo Yu
Journal: Oncology letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: Rho-associated protein kinase 1; metastasis; microRNA-150; osteosarcoma; tumor suppressor.
Affiliations: Department of Orthopedics, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China., Department of Orthopedics, People's Hospital of Rizhao, Rizhao, Shandong 276826, P.R. China.

Abstract:  Osteosarcoma (OS) is the most common form of bone malignancy in children and adolescents. A class of molecules known as microRNAs (miRNAs) have been routinely associated in the development and progression of OS. The present study was centered on the less well-known miRNA, miRNA (miR)-150, and its role in OS was investigated. The levels of miR-150 were examined in 40 tissue specimens from patients with OS and adjacent normal tissues using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis. In addition the expression levels of miR-150 were examined in three OS cell lines and a normal osteoblast cell line. Cell proliferation, migration and invasion assays were performed to establish the correlation between miR-150 and metastasis. The potential targets of miR-150 were theoretically predicted and one high-scoring target, Rho-associated kinase 1 (ROCK1), was established to be a direct target using RT-qPCR and western blot analyses and Pearson's correlation analysis. The results indicated that miR-150 was downregulated in tissues from patients with OS and cell lines. Secondly, it was shown that the overexpression of miR-150 was inversely correlated with OS cell proliferation, migration and invasion. It was also shown that miR-150 negatively regulated the gene expression of ROCK1 in the OS cell lines. Finally, the interaction between miR-150 and ROCK1 was established and it was shown that miR-150 directly targeted ROCK1. In conclusion, miR-150 was found to be a tumor suppressor, and the suppression of miR-150 resulted in elevation in the levels of ROCK1. This interaction between miR-150 and ROCK1 may be key in the progression of OS. Furthermore, miR-150 or ROCK1 may be potential therapeutic targets for the treatment of OS. 

Retracted: No

PubPeer comments:
 Image concerns in this paper were found during a systematic search of papers in Spandidos journals for possible duplicated images. Figure 3. * Red boxes: The  SaOS2-NC Migration and  SaOS2 miR-1500 Invasion panels appear to show an overlap. ![file] , 
 Figure 4B. * Blue boxes: The three beta-actin panels, each representing a different cell line, appear to look similar, albeit stretched differently. ![file] , 
 #1 Fig 3 again. ![file] The orange box marks a panel that previously appeared in - *[left]* Fig 4A B of  B7-H1 Expression Is Associated with Poor Prognosis in Colorectal Carcinoma and Regulates the Proliferation and Invasion of HCT116 Colorectal Cancer Cells ([Shi et al 2013] ). - *[right]* Fig 4a b of  TRIM29 as a Novel Biomarker in Pancreatic Adenocarcinoma ([Sun et al 2014] ). ![file] , 
 Retracted [17 August 2022] .  Following the publication of the above paper, a concerned reader drew to the Editors attention that the Transwell cell migration and invasion assay data shown in Fig. 3C appeared to overlap in a pair of the data panels within this figure; in addition, data that were strikingly similar to those included in this figure had already appeared in previously published papers written by different authors at different institutes. Moreover, there was an unexpected level of similarity regarding the control u03b2u2011actin bands shown in the three western blot experiments in Fig. 4B, even though these experiments related to three different cell lines. Having considered the issues identified, the Editor of Oncology Letters has decided that this article should be retracted from the Journal on account of the previously published data, and uncertainties regarding other data in Figs. 3 and 4. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. ,