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Increased miR-214 expression suppresses cell migration and proliferation in Hirschsprung disease by interacting with PLAGL2

BACKGROUND: The miR-214 has been reported to be associated with various diseases, but its involvement in the pathophysiology of Hirschsprung disease (HSCR) is almost completely unexplored. METHODS: In our study, we conducted a series of experiments to unravel the biological role of miR-214 in the pa...

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Detalles Bibliográficos
Autores principales: Wu, Liang, Yuan, Wenzheng, Chen, Jinhuang, Zhou, Zili, Shu, Yan, Ji, Jintong, Liu, Zhengyi, Tang, Qiang, Zhang, Xudan, Shu, Xiaogang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group US 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6768286/
https://www.ncbi.nlm.nih.gov/pubmed/30822775
http://dx.doi.org/10.1038/s41390-019-0324-9
Descripción
Sumario:BACKGROUND: The miR-214 has been reported to be associated with various diseases, but its involvement in the pathophysiology of Hirschsprung disease (HSCR) is almost completely unexplored. METHODS: In our study, we conducted a series of experiments to unravel the biological role of miR-214 in the pathophysiology of HSCR. qRT-PCR and western blotting were utilized to investigate the relative expression levels of miR-214, mRNAs, and proteins of related genes in colon tissues from 20 controls without HSCR and 24 patients with HSCR. The potential biological role of miR-214 in two cell lines (SKN-SH and SH-SY5Y) was assessed using the CCK8 assay, EdU staining, transwell assay, and flow cytometry. The dual-luciferase reporter assay was used to confirm PLAGL2 as a common target gene of miR-214. RESULTS: All results suggested that miR-214 is upregulated in HSCR tissue samples compared with controls. Additionally, we found that miR-214 could inhibit cell proliferation and migration by directly downregulating the expression of PLAGL2, and the extent of the miR-214-mediated inhibitory effects could be rescued by a PLAGL2 overexpression plasmid. CONCLUSION: Our results revealed that miR-214 is indeed involved in the pathophysiology of HSCR and suppresses cell proliferation and migration by directly downregulating PLAGL2 in cell models.