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miR-202-5p inhibits the migration and invasion of osteosarcoma cells by targeting ROCK1

Many studies have shown that microRNA regulates the development and treatment of osteosarcoma (OS). In many human cancer studies, the expression of microRNA-202 has been shown to be abnormal. The aim of the study was to examine the role of miR-202-5p in the occurrence and formation of OS. miR-202-5p...

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Detalles Bibliográficos
Autores principales: Li, Congda, Ma, Deying, Yang, Jinhu, Lin, Xiangbo, Chen, Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6019893/
https://www.ncbi.nlm.nih.gov/pubmed/29963151
http://dx.doi.org/10.3892/ol.2018.8694
Descripción
Sumario:Many studies have shown that microRNA regulates the development and treatment of osteosarcoma (OS). In many human cancer studies, the expression of microRNA-202 has been shown to be abnormal. The aim of the study was to examine the role of miR-202-5p in the occurrence and formation of OS. miR-202-5p and Rho-associated coiled-coil containing protein kinase 1 (ROCK1) levels were assessed using RT-qPCR in OS tissues and cell lines. The cell migrating and invasive abilities were detected by the Transwell assay in OS. Moreover, the relationship between miR-202-5p and ROCK1 was verified via luciferase reporter assay. The protein level of ROCK1 was identified by western blot analysis. Downregulation of miR-202-5p was identified in OS tissues and cell lines. In addition, the miR-202-5p overexpression had inhibitory action for cell migration and invasion in OS. Moreover, miR-202-5p directly targeted ROCK1 and negatively regulated its expression. Upregulation of ROCK1 had a carcinogenic effect in OS. Furthermore, the upregulation of ROCK1 restored the suppressive effect of miR-202-5p. miR-202-5p, in turn, weakened the abilities of cell migration and invasion in OS by inhibiting ROCK1 expression. As a result, miR-202-5p may be developed as a potential pathway in the reatment of OS.