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MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway

BACKGROUND: Oral carcinoma, one of the most commonly diagnosed cancers, has a poor prognosis and low survival rate with treatment. In recent years, some studies reported the upregulation of miRNA-16 (miR-16) in the oral carcinoma, whereas some other studies confirmed the downregulation of miR-16. In...

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Detalles Bibliográficos
Autores principales: Liu, Lijun, Jiang, Han, Zhao, Jin, Wen, Hao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6112799/
https://www.ncbi.nlm.nih.gov/pubmed/30197522
http://dx.doi.org/10.2147/OTT.S153888
Descripción
Sumario:BACKGROUND: Oral carcinoma, one of the most commonly diagnosed cancers, has a poor prognosis and low survival rate with treatment. In recent years, some studies reported the upregulation of miRNA-16 (miR-16) in the oral carcinoma, whereas some other studies confirmed the downregulation of miR-16. In the current study, we aimed to investigate the function of miR-16 in oral carcinoma. MATERIALS AND METHODS: Cell proliferation assay was measured by MTT assay, quantitative real time polymerase chain reaction (qRT-PCR) was used to evaluate the expression of miR-16, and apoptosis was analyzed by flow cytometry. In addition, the expression of proteins was detected by Western blot. Moreover, xenograft tumor model was established to detect the effect of miR-16 in vivo. RESULTS: The results suggested that miR-16 was downregulated in the oral carcinoma tissues. Overexpression of miR-16 inhibited the growth and proliferation of oral squamous carcinoma cells (OSCCs) and induced apoptosis both in vitro and in vivo, which is due to the suppression of Wnt/β-catenin signaling pathway. CONCLUSION: This study provides evidence that overexpression of miR-16 inhibits OSCC growth by regulating Wnt/β-catenin signaling. Our findings suggest that overexpression of miR-16 could be a potential approach for gene therapy of OSCC in future.