MNX1-AS1 accelerates the epithelial-mesenchymal transition in osteosarcoma cells by activating MNX1 as a functional oncogene.
Eur Rev Med Pharmacol Sci
; 23(19): 8194-8202, 2019 Oct.
Article
en En
| MEDLINE
| ID: mdl-31646549
ABSTRACT
OBJECTIVE:
To investigate whether MNX1-AS1 can accelerate epithelial-mesenchymal transition (EMT) of osteosarcoma cells via activating MNX1. PATIENTS ANDMETHODS:
The expression pattern of MNX1-AS1 in osteosarcoma tissues and cell lines was examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, the cytoplasmic and nuclear levels of MNX1-AS1 in osteosarcoma cells were also determined. The regulatory effects of MNX1-AS1 on viability, clonality, migratory, and invasive abilities of the osteosarcoma cells were evaluated. The relative levels of MNX1 and EMT-related genes influenced by MNX1-AS1 were detected. The methylation ability in the promoter of the osteosarcoma cells transfected with si-MNX1-AS1 or MNX1-AS1 vector was determined by the whole genome bisulfite sequencing.RESULTS:
MNX1-AS1 was upregulated in osteosarcoma tissues and cell lines, which was mainly expressed in the nucleus. The knockdown of MNX1-AS1 markedly attenuated viability, clonality, migratory, and the invasive abilities of the osteosarcoma cells. Besides, the transfection of si-MNX1-AS1 in U2OS and MG63 cells downregulated MNX1 and Snail, and upregulated E-cadherin. The methylation ability increased after the knockdown of MNX1-AS1, while the overexpression of MNX1-AS1 obtained the opposite trends.CONCLUSIONS:
MNX1-AS1 mediates EMT of the osteosarcoma cells via activating MNX1, thereafter accelerating the progression of the osteosarcoma.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Factores de Transcripción
/
Neoplasias Óseas
/
Osteosarcoma
/
Proteínas de Homeodominio
/
Transición Epitelial-Mesenquimal
Límite:
Humans
Idioma:
En
Revista:
Eur Rev Med Pharmacol Sci
Asunto de la revista:
FARMACOLOGIA
/
TOXICOLOGIA
Año:
2019
Tipo del documento:
Article
País de afiliación:
China