MicroRNA‑130a inhibits growth and metastasis of osteosarcoma cells by directly targeting ZEB1 Retraction in /10.3892/mmr.2022.12756

Yi,Lankai; Liu,Meixiu; Tang,Zhiliang

doi:10.3892/mmr.2017.6968

MicroRNA‑130a inhibits growth and metastasis of osteosarcoma cells by directly targeting ZEB1

Retraction in: /10.3892/mmr.2022.12756

Authors:
- Lankai Yi
- Meixiu Liu
- Zhiliang Tang
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Affiliations: Department of Hand and Feet Surgery, Weifang People's Hospital, Weifang, Shandong 261000, P.R. China, Department of Orthopedics, An Qiu People's Hospital, Anqiu, Shandong 262100, P.R. China
Published online on: July 13, 2017 https://doi.org/10.3892/mmr.2017.6968
Pages: 3606-3612

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Abstract

Osteosarcoma (OS) is the most common malignant bone tumor in children and adolescents. microRNAs (miRNAs) have previously been reported to be involved in the carcinogenesis and progression of OS, and may be useful prognostic markers or therapeutic targets for patients with OS. miRNA‑130a has been previously studied in multiple types of human cancer. However, its expression and function in OS has not been well documented. The aim of the present study was to investigate the expression, biological functions and molecular mechanisms underlying the effect of miR‑130a in OS. miR‑130a was significantly downregulated in OS tissues and cell lines compared with normal bone tissue and a normal osteoblast cell line. miR‑130a expression levels was significantly negatively correlated with the clinical stage and metastasis of OS. Further studies indicated that overexpression of miR‑130a inhibited OS cell proliferation, migration and invasion in vivo. In terms of the mechanisms underlying this effect, zinc finger E‑box binding homeobox 1 (ZEB1) was demonstrated to act as a direct target of miR‑130a in OS. Furthermore, downregulation of ZEB1 by interference with small interfering RNA mimicked the effects of transfection with an miR‑130a mimic in OS. In conclusion, these results demonstrated that miR‑130a functioned as a tumor suppressor in OS, partially via targeting ZEB1, suggesting that miR‑130a may be considered as a target for the treatment of patients with OS.

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