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miR-577 suppresses cell proliferation and epithelial-mesenchymal transition by regulating the WNT2B mediated Wnt/β-catenin pathway in non-small cell lung cancer

MicroRNAs (miRNAs/miRs) serve important roles in regulating malignant phenotype in numerous cancers, such as non-small cell lung cancer (NSCLC); however, the role and function of miR-577 in NSCLC remains unknown. In the present study, miR-577 expression levels were observed to be downregulated in NS...

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Detalles Bibliográficos
Autores principales: Wang, Bin, Sun, Liwei, Li, Jinduo, Jiang, Rong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6102634/
https://www.ncbi.nlm.nih.gov/pubmed/30015869
http://dx.doi.org/10.3892/mmr.2018.9279
Descripción
Sumario:MicroRNAs (miRNAs/miRs) serve important roles in regulating malignant phenotype in numerous cancers, such as non-small cell lung cancer (NSCLC); however, the role and function of miR-577 in NSCLC remains unknown. In the present study, miR-577 expression levels were observed to be downregulated in NSCLC via reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assay, and inhibited cell proliferation, cell migration and invasion and epithelial-mesenchymal transition progress in NSCLC cells. The predicted target genes of miR-577 were determined by enhanced green fluorescent protein reporter assay, RT-qPCR and western blot analyses. miR-577 was demonstrated to suppress the expression of WNT2B by targeting the 3′-untranslated region of WNT2B mRNA in H522 and A549 cells. WNT2B was upregulated in NSCLC cells as observed via RT-qPCR analysis, and the malignant phenotype of H522 and A549 cells were promoted by WNT2B overexpression. In addition, miR-577 inactivated the Wnt/β-catenin pathway by targeting WNT2B in NSCLC cells. Collectively, miR-577 may function as a suppressor gene by directly downregulatingWNT2B mRNA and protein expression levels in H522 and A549 cells, and may serve important roles in the malignancy of NSCLC.