The role and mechanism of microRNA‑18a‑5p in oral squamous cell carcinoma
Autor: | Linfeng Lai, Chenyao Huang, Hongning Song |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Cancer Research Cell Vimentin migration Biochemistry SMAD2 03 medical and health sciences 0302 clinical medicine Cell Movement Cell Line Tumor microRNA Genetics medicine Humans Neoplasm Invasiveness Viability assay Molecular Biology biology Oncogene Chemistry miR-18a-5p apoptosis Articles Cell cycle invasion Gene Expression Regulation Neoplastic oral squamous cell carcinoma stomatognathic diseases MicroRNAs 030104 developmental biology medicine.anatomical_structure Oncology Cell culture Apoptosis 030220 oncology & carcinogenesis biology.protein Cancer research Carcinoma Squamous Cell Molecular Medicine Mouth Neoplasms |
Zdroj: | Molecular Medicine Reports |
ISSN: | 1791-3004 |
Popis: | 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. |
Databáze: | OpenAIRE |
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