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The role and mechanism of microRNA-18a-5p in oral squamous cell carcinoma

The purpose of this study was mainly to explore the role and mechanism of microRNA-18a-5p (miR-18a-5p) in oral squamous cell carcinoma (OSCC). The expression of miR-18a-5p in OSCC cells and normal cells was firstly detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR)...

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Detalles Bibliográficos
Autores principales: Huang, Chenyao, Song, Hongning, Lai, Linfeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6625443/
https://www.ncbi.nlm.nih.gov/pubmed/31257489
http://dx.doi.org/10.3892/mmr.2019.10403
Descripción
Sumario:The purpose of this study was mainly to explore the role and mechanism of microRNA-18a-5p (miR-18a-5p) in oral squamous cell carcinoma (OSCC). The expression of miR-18a-5p in OSCC cells and normal cells was firstly detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The cell viability, apoptosis, migration and invasion abilities of OSCC cells were determined by MTT, cell apoptosis, wound healing and Transwell assays respectively. Additionally, bioinformatics software analysis and luciferase reporter assays were performed to predict and confirm the candidate target of miR-18a-5p. Western blot analysis was used to assess protein expression. It was revealed that the expression of miR-18a-5p in OSCC cells was higher than that in normal cells. In vitro studies revealed that the cell viability, migration and invasion abilities of OSCC cells were promoted and cell apoptosis was inhibited by miR-18a-5p overexpression. In addition, Smad2 was identified as a target of miR-18a-5p. It was also revealed that miR-18a-5p overexpression significantly inhibited the expression of Smad2, Smad4 and E-cadherin, and the levels of Smad7, collagen I, transforming growth factor-β (TGF-β), α-smooth muscle actin (α-SMA), vimentin were enhanced. While miR-18a-5p downregulation presented the opposite effects. In conclusion, the results indicated that miR-18a-5p can regulate the biological process of OSCC by targeting Smad2 and miR-18a-5p/Smad2 may be potential therapeutic targets for OSCC.