4.5 Article

miR-34a inhibits proliferation, migration and invasion of paediatric neuroblastoma cells via targeting HNF4α

Journal

ARTIFICIAL CELLS NANOMEDICINE AND BIOTECHNOLOGY
Volume 47, Issue 1, Pages 3072-3078

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.1080/21691401.2019.1637886

Keywords

miR-34a; neuroblastoma; hepatocyte nuclear factor 4 alpha; migration; invasion

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Objective: To investigate the potential mechanism of microRNA-34a (miR-34a) on proliferation, migration and invasion of paediatric neuroblastoma cells. Methods: The expression of miR-34a and hepatocyte nuclear factor 4 alpha (HNF4 alpha) in paediatric neuroblastoma tissues were detected by RT-q PCR and Western blot, respectively. Cell proliferation, migration, invasion and the expression of matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 14 (MMP-14) after transfection of miR-34a mimics or HNF4 alpha siRNA into SH-SY5Y cells were detected by MTT assay, Transwell assay and Western blot assay, respectively. The target relationship between miR-34a and HNF4 alpha was verified by TargetScan online prediction and dual-luciferase assay. Cell proliferation, migration and invasion of SH-SY5Y cells after overexpression of miR-34a and HNF4 alpha were detected. Results: The expression level of miR-34a was decreased (p < .05) while the expression level of HNF4 alpha was increased (p < .05) in paediatric neuroblastoma tissues. Over-expression of Mi-34a or knockdown of HNF4 alpha in SH-SY5Y cells could lead to a decreased of cell proliferation, migration, invasion and the expression of MMP-2 and MMP-14 (p < .05). The results of TargetScan online prediction and dual-luciferase assay indicted that HNF4 alpha was a potential target gene for miR-34a. Overexpression of HNF4 alpha could reverse the inhibition of miR-34a on proliferation, migration and invasion of SH-SY5Y cells. Conclusion: The expression of miR-34a was down-regulated in paediatric neuroblastoma tissues, and overexpression of miR-34a could inhibit proliferation, migration and invasion of SH-SY5Y cells by targeting HNF4 alpha.

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