MicroRNA‑101 has a suppressive role in osteosarcoma cells through the targeting of c‑FOS Retraction in /10.3892/etm.2021.10410

Wang,Zili; He,Rongzhen; Xia,Hansong; Wei,Yu; Wu,Song

doi:10.3892/etm.2016.3085

MicroRNA‑101 has a suppressive role in osteosarcoma cells through the targeting of c‑FOS

Retraction in: /10.3892/etm.2021.10410

Authors:
- Zili Wang
- Rongzhen He
- Hansong Xia
- Yu Wei
- Song Wu
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Affiliations: Department of Orthopaedic Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China
Published online on: February 17, 2016 https://doi.org/10.3892/etm.2016.3085
Pages: 1293-1299
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

MicroRNAs (miRs) have been implicated in the development and progression of osteosarcoma (OS). However, the underlying mechanism of miR‑101 in regulating of the proliferation, migration and invasion of OS cells remains to be elucidated. In the present study, reverse transcription‑quantitative polymerase chain reaction data revealed that miR‑101 was frequently downregulated in the tissue samples of 12 patients with OS compared with their matched adjacent non‑tumor tissues. Furthermore, miR‑101 was significantly downregulated in three common OS cell lines, Saos‑2, MG63 and U2OS, compared with the human osteoblast cell line, hFOB1.19 (P<0.01). A luciferase reporter assay was also performed and identified c‑FOS as a novel target of miR‑101 in U2OS cells; overexpression of miR‑101 significantly suppressed the protein expression levels of c‑FOS, while knockdown of miR‑101 significantly enhanced the formers' expression levels in U2OS cells (P<0.01). Independent inhibition of c‑FOS and overexpression of miR‑101 expression levels significantly suppressed U2OS cell proliferation, migration and invasion (P<0.01). However, overexpression of c‑FOS reversed the inhibitory effect of miR‑101 upregulation on proliferation, migration and invasion of U2OS cells, suggesting that miR‑101 acts as a tumor suppressor in OS cells via targeting of c‑FOS. Thus, we propose that the miR‑101/c‑FOS axis may be a potential therapeutic target for OS.

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