MiR-329-3p inhibits hepatocellular carcinoma cell proliferation and migration through USP22-Wnt/ß-Catenin pathway.
Eur Rev Med Pharmacol Sci
; 24(19): 9932-9939, 2020 10.
Article
em En
| MEDLINE
| ID: mdl-33090397
ABSTRACT
OBJECTIVE:
MicroRNA-329-3p (miR-329-3p) has been shown to be involved in tumor development. But its role in hepatocellular carcinoma has not been explored. Our study aims to explore the effect and mechanism of miR-329-3p on hepatocellular carcinoma development. PATIENTS ANDMETHODS:
Hepatocellular carcinoma tissues and paired paracancerous specimens from 31 hepatocellular carcinoma patients undergoing surgery were collected. Quantitative real-time polymerase chain reaction and Western blot were employed to measure genes expression at mRNA and protein level. CCK-8 and transwell assays were performed to evaluate hepatocellular carcinoma cells proliferation and migration. Dual-Luciferase reporter gene assay was designed to validate the target gene of miR-329-3p.RESULTS:
Our study showed miR-329-3p expression was significantly lower in hepatocellular carcinoma tissue. MiR-329-3p mimic inhibits proliferation and migration of HepG2 cells. By using Dual-Luciferase reporter gene assay, we proved that miR-329-3p inhibited HepG2 cell proliferation and migration by targeting USP22 directly. By up- and downregulation of USP22 expression, we also proved that USP22 can activate the Wnt/ß-Catenin pathway, which in turn affected the proliferation and migration of HepG2 cells.CONCLUSIONS:
We demonstrated that miR-329-3p can inhibit HepG2 cell proliferation and migration by inhibiting USP22-Wnt/ß-Catenin pathway. Our study provides novel insights into the aetiology and potential treatment of hepatocellular carcinoma.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Carcinoma Hepatocelular
/
MicroRNAs
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Ubiquitina Tiolesterase
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Beta Catenina
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Neoplasias Hepáticas
Limite:
Humans
Idioma:
En
Revista:
Eur Rev Med Pharmacol Sci
Assunto da revista:
FARMACOLOGIA
/
TOXICOLOGIA
Ano de publicação:
2020
Tipo de documento:
Article