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MicroRNA-744 promotes carcinogenesis in osteosarcoma through targeting LATS2

Osteosarcoma (OS) mortality rate is increasing. Various microRNAs (miRNAs) have been investigated in the pathological process of OS except for miR-744. Hence, this research was designed to explore miR-744 function in OS. RT-qPCR and western blot analysis were used to quantify miR-744 and large tumor...

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Detalles Bibliográficos
Autores principales: Sun, Liangzhi, Liu, Ming, Luan, Suxian, Shi, Yulin, Wang, Qiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676671/
https://www.ncbi.nlm.nih.gov/pubmed/31452740
http://dx.doi.org/10.3892/ol.2019.10530
Descripción
Sumario:Osteosarcoma (OS) mortality rate is increasing. Various microRNAs (miRNAs) have been investigated in the pathological process of OS except for miR-744. Hence, this research was designed to explore miR-744 function in OS. RT-qPCR and western blot analysis were used to quantify miR-744 and large tumor suppressor kinase 2 (LATS2) expression levels. The function of miR-744 was investigated using MTT and Transwell assays. Target gene of miR-744 was verified by dual-luciferase reporter assay. miR-744 expression was increased in OS, which was associated with worse clinical features and prognosis of OS patients. Importantly, miR-744 promoted cell viability and metastasis in OS. Furthermore, miR-744 induced Wnt/β-catenin pathway and epithelial-mesenchymal transition (EMT) in OS. In addition, miR-744 directly targeted LATS2 and blocked its expression in OS. Moreover, upregulation of LATS2 weakened the promotion of cell viability and metastasis induced by miR-744 in OS. In conclusion, miR-744 accelerated OS progression through restraining LATS2 and activating Wnt/β-catenin pathway and EMT.