The Long Noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript-1 Regulates CCDC80 Expression by Targeting miR-141-3p/miR-200a-3p in Vascular Smooth Muscle Cells.
J Cardiovasc Pharmacol
; 75(4): 336-343, 2020 04.
Article
en En
| MEDLINE
| ID: mdl-31934911
ABSTRACT
OBJECTIVE:
Our previous study showed that Coiled-Coil Domain Containing 80 (CCDC80) accelerates the development of atherosclerosis by decreasing lipoprotein lipase (LPL) expression and activity in apoE knockout mice. However, the regulatory mechanism for CCDC80 expression is unclear. This study was designed to evaluate whether noncoding RNAs involved the regulation of CCDC80 expression in vascular smooth muscle cells. METHODS ANDRESULTS:
Bioinformatics prediction and luciferase reporter gene results showed that miR-141-3p/200a-3p bound to the 3'UTR of CCDC80. Furthermore, miR-141-3p/200a-3p mimics decreased the expression of CCDC80 but increased LPL expression. Opposite results were observed with miR-141-3p/200a-3p inhibitors. We also found that lncRNA metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) interacted with the sequences of miR-141-3p/200a-3p and decreased their expression. RT-qPCR and western blotting results showed that MALAT1 overexpression increased CCDC80 expression and decreased LPL expression, while MALAT1 knockdown displayed an opposite phenotype. The effects of both MALAT1 overexpression and knockdown were blocked by miR-141-3p/200a-3p mimics or inhibitors.CONCLUSIONS:
Thus, we demonstrated that lncRNA MALAT1 regulates CCDC80 and LPL expression through miR-141-3p/200a-3p.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Proteínas de la Matriz Extracelular
/
Miocitos del Músculo Liso
/
MicroARNs
/
ARN Largo no Codificante
/
Músculo Liso Vascular
Tipo de estudio:
Prognostic_studies
/
Risk_factors_studies
Límite:
Humans
Idioma:
En
Revista:
J Cardiovasc Pharmacol
Año:
2020
Tipo del documento:
Article
País de afiliación:
China