miR‑34c‑3p acts as a tumor suppressor gene in osteosarcoma by targeting MARCKS

Liu,Hongliang; Su,Pengxiao; Zhi,Liqiang; Zhao,Kai

doi:10.3892/mmr.2017.6108

miR‑34c‑3p acts as a tumor suppressor gene in osteosarcoma by targeting MARCKS

Authors:
- Hongliang Liu
- Pengxiao Su
- Liqiang Zhi
- Kai Zhao
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Affiliations: Department of Foot and Ankle Surgery, Xi'an Honghui Hospital, Xi'an, Shanxi 710054, P.R. China, Department of Surgery, Xi'an Honghui Hospital, Xi'an, Shanxi 710054, P.R. China, Department of Articular Orthopedics, Xi'an Honghui Hospital, Xi'an, Shanxi 710054, P.R. China
Published online on: January 11, 2017 https://doi.org/10.3892/mmr.2017.6108
Pages: 1204-1210
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Previous studies have demonstrated that microRNA (miR)‑34c‑3p is important in human cancer progression. However, the function of miR‑34c‑3p in osteosarcoma (OS) remains to be elucidated. In the present study, miR‑34c‑3p level was measured by reverse transcription‑quantitative polymerase chain reaction in OS tissues and the associated prognostic value for overall survival was determined. The function of miR‑34c‑3p was examined in vitro and in vivo. A luciferase reporter assay was used to identify the targets of miR‑34c‑3p. The results of the present study revealed that miR‑34c‑3p was downregulated in OS tissues and cell lines, and decreased levels of miR‑34c‑3p were associated with a high mortality rate in patients with OS. Furthermore, restoration of miR‑34c‑3p expression reduced cell growth in vitro and suppressed tumorigenesis in vivo. Conversely, inhibition of miR‑34c‑3p stimulated OS cell growth in vitro and in vivo. Myristoylated alanine‑rich protein kinase C substrate (MARCKS) was identified as a direct target of miR‑34c‑3p and its overexpression partly reversed the suppressive effects of miR‑34c‑3p. Furthermore, MARCKS was revealed to be upregulated and inversely correlated with miR‑34c‑3p levels in OS tissues. These data suggested that miR‑34c‑3p acts as a tumor suppressor via regulation of MARCKS expression in OS progression and miR‑34c‑3p may be a promising therapeutic target for this type of cancer.

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