microRNA-18a Promotes Cell Migration and Invasion Through Inhibiting Dicer l Expression in Hepatocellular Carcinoma In Vitro / 中国医学科学杂志(英文版)
Chinese Medical Sciences Journal
;
(4): 34-33, 2017.
Artigo
em Inglês
| WPRIM
| ID: wpr-281421
ABSTRACT
Objective To investigate the effects of microRNA-18a (miR-18a) on migration and invasion of hepatocellular carcinoma (HCC) cells, and its possible mechanism associated with Dicer l.Methods HepG2 and HepG2.2.15 cells were transfected with miR-18a inhibitor using Lipofectamine. Cell invasion was evaluated by transwell invasion assay, and cell migration was detected by transwell migration and wound-healing assays. Moreover, luciferase reporter assay was used to identify whether Dicer expression was regulated by miR-18a. Real-time RT-PCR and western blot were performed to analyze Dicer 1 expression. In addition, a functional restoration assay was performed to investigate whether miR-18a promotes HCC cell migration and invasion by directly targeting Dicer 1.Results miR-18a inhibitor can suppress the migration and invasion of HCC cells. Furthermore, suppression of Dicer l expression by small interfering RNA essentially abolished the inhibition of cell migration and invasion induced by miR-18a inhibitor, restorating these activities to levels similar to the parental HCC cells. Interestingly, suppression of miR-18a in HCC cells resulted in enhanced expression of Dicer l. In addition, the results of a luciferase assay demonstrated targeted regulation of Dicer l by miR-18a.Conclusion Our findings suggest that miR-18a promotes migration and invasion of HCC cells by inhibiting Dicer l expression.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
RNA Neoplásico
/
Movimento Celular
/
Carcinoma Hepatocelular
/
MicroRNAs
/
Ribonuclease III
/
RNA Helicases DEAD-box
/
Células Hep G2
/
Genética
/
Neoplasias Hepáticas
Tipo de estudo:
Estudo prognóstico
Limite:
Humanos
Idioma:
Inglês
Revista:
Chinese Medical Sciences Journal
Ano de publicação:
2017
Tipo de documento:
Artigo
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