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

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 reacti...

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Detalles Bibliográficos
Autores principales: Liu, Hongliang, Su, Pengxiao, Zhi, Liqiang, Zhao, Kai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5367338/
https://www.ncbi.nlm.nih.gov/pubmed/28075441
http://dx.doi.org/10.3892/mmr.2017.6108
Descripción
Sumario: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.