MicroRNA-1236-3p inhibits proliferation and invasion of breast cancer cells by targeting ZEB1.
Eur Rev Med Pharmacol Sci
; 23(22): 9988-9995, 2019 Nov.
Article
en En
| MEDLINE
| ID: mdl-31799668
ABSTRACT
OBJECTIVE:
This research aims to investigate the level of microRNA-1236-3p in breast cancer (BCa) tissues and to further investigate its possible mechanism in the progression of BCa. PATIENTS ANDMETHODS:
The level of microRNA-1236-3p in BCa tissues and adjacent tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). Regulatory effects of microRNA-1236-3p on cell proliferation and invasion were detected by cell counting kit-8 (CCK-8) and transwell assay. The binding relationship between microRNA-1236-3p and zinc-finger E-box binding homeobox (ZEB1) was examined by the dual-luciferase reporter gene assay. Finally, rescue experiments were conducted to verify the potential role of microRNA-1236-3p/ ZEB1 axis in BCa.RESULTS:
MicroRNA-1236-3p was downregulated in BCa tissues relative to adjacent tissues, and the similar trend was shown in BCa cell lines. Overexpression of microRNA-1236-3p in MDA-MB-231 and MCF-7 cells inhibited proliferation and attenuated invasiveness, while knockdown of microRNA-1236-3p had an opposite effect. Dual-luciferase reporter gene assay and qRT-PCR results showed that microRNA-1236-3p could target ZEB1 to degrade it. Overexpression of ZEB1 in BCa cells can partially reverse the effect of overexpressed miR-1236-3p on cell proliferative and invasive abilities.CONCLUSIONS:
MicroRNA-1236-3p could inhibit the growth and metastasis of BCa cells by inhibiting ZEB1 expression, suggesting that microRNA-1236-3p may be a potential therapeutic target for BCa.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neoplasias de la Mama
/
Regulación hacia Abajo
/
MicroARNs
/
Homeobox 1 de Unión a la E-Box con Dedos de Zinc
Límite:
Female
/
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