miR-150 is downregulated in osteosarcoma and suppresses cell proliferation, migration and invasion by targeting ROCK1
Retraction in: /10.3892/ol.2022.13462
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- Published online on: February 9, 2017 https://doi.org/10.3892/ol.2017.5709
- Pages: 2191-2197
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Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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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.