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Study of miR-10b regulatory mechanism for epithelial-mesenchymal transition, invasion and migration in nasopharyngeal carcinoma cells

The aim of the study was to investigate the miR-10b regulatory mechanism for epithelial-mesenchymal transition (EMT) and its effect on the proliferation and migration of nasopharyngeal carcinoma cells. RT-qPCR was used to detect the expression of miR-10b in CNE1 nasopharyngeal carcinoma cell line. T...

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Detalles Bibliográficos
Autor principal: Wang, Weiyi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5754829/
https://www.ncbi.nlm.nih.gov/pubmed/29344154
http://dx.doi.org/10.3892/ol.2017.7172
Descripción
Sumario:The aim of the study was to investigate the miR-10b regulatory mechanism for epithelial-mesenchymal transition (EMT) and its effect on the proliferation and migration of nasopharyngeal carcinoma cells. RT-qPCR was used to detect the expression of miR-10b in CNE1 nasopharyngeal carcinoma cell line. The NP69 nasopharyngeal mucosal cell line was used to determine the expression of miR-10b after infection with lentivirus. The effect of miR-10b on the proliferation of NP69 was examined using cell counting kit-8. The effect of miR-10b on NP69 migration was examined using scratch assay. Western blot analysis was used to detect the effects of miR-10b on the expression of epithelial cell markers E-cadherin and β-catenin and mesenchymal cell markers fibronectin, N-cadherin, vimentin and matrix metalloproteinase-9 (MMP-9). The present study showed that miR-10b was highly expressed in CNE1 cells. The stable expression of miR-10b promoted the proliferation and migration of NP69 cells, downregulated the expression of epithelial cell markers E-cadherin and β-catenin, and upregulated the expression of mesenchymal cell markers fibronectin, N-cadherin, vimentin and MMP-9 resulting in cell EMT. In conclusion, miR-10b promotes the proliferation and migration of nasopharyngeal carcinoma cells, and induces EMT in nasopharyngeal carcinoma cells, thereby having the potential to become a new target for the treatment of nasopharyngeal carcinoma.