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MicroRNA-20a promotes the proliferation and cell cycle of human osteosarcoma cells by suppressing early growth response 2 expression

MicroRNAs (miRNAs) are crucial in cancer development. However, the underlying mechanisms of miRNAs in osteosarcoma (OS) remain largely uncharacterized. The present study investigated the role of miR-20a in OS cell proliferation. It was determined that miR-20a expression is markedly upregulated in OS...

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Detalles Bibliográficos
Autores principales: ZHUO, WENKUN, GE, WEIMING, MENG, GUOLIN, JIA, SHUAIJUN, ZHOU, XIANG, LIU, JIAN
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4581803/
https://www.ncbi.nlm.nih.gov/pubmed/26238942
http://dx.doi.org/10.3892/mmr.2015.4098
Descripción
Sumario:MicroRNAs (miRNAs) are crucial in cancer development. However, the underlying mechanisms of miRNAs in osteosarcoma (OS) remain largely uncharacterized. The present study investigated the role of miR-20a in OS cell proliferation. It was determined that miR-20a expression is markedly upregulated in OS tissues and cells compared with the matched adjacent normal tissues and h-FOB human osteoblast cell lines. Ectopic expression of miR-20a promoted the proliferation and anchorage-independent growth of OS cells, whereas inhibition of miR-20a reduced this effect. Bioinformatics analysis further revealed early growth response 2 (EGR2), as a potential target of miR-20a. Data from luciferase reporter assays showed that miR-20a directly binds to the 3′-untranslated region (3′-UTR) of EGR2 mRNA and represses expression at the transcriptional and translational levels. In functional assays, miR-20a promoted OS cell proliferation and the cell cycle, which could be suppressed by an inhibitor of miR-20a. In conclusion, the data provide compelling evidence that miR-20a functions as an onco-miRNA, which is important in promoting cell proliferation in OS, and its oncogenic effect is mediated primarily through direct suppression of EGR2 expression.