Circular RNA circ_0001955 promotes hepatocellular carcinoma tumorigenesis by up-regulating alkaline ceramidase 3 expression through microRNA-655-3p.
Bioengineered
; 13(2): 2099-2113, 2022 02.
Article
en En
| MEDLINE
| ID: mdl-35034572
The involvement of certain circular RNAs (circRNAs) in the development of hepatocellular carcinoma (HCC) has been reported. Herein, this study aimed to investigate the function and mechanism of circ_0001955 in HCC tumorigenesis. Expression of circ_0001955, miR-655-3p, and alkaline ceramidase 3 (ACER3) was evaluated by quantitative real-time PCR and Western blot. Cell counting kit-8, colony formation, transwell, tube formation, flow cytometry and tumor xenograft assays were adopted to perform in vitro and in vivo experiments. The direct interaction between miR-655-3p and circ_0001955 or ACER3 was verified using dual-luciferase reporter and RNA immunoprecipitation assays. Circ_0001955 was highly expression in HCC tissues and cells. Functionally, circ_0001955 deletion suppressed HCC tumorigenesis in vitro by suppressing cell growth, metastasis and angiogenesis. Mechanistically, circ_0001955 could competitively sponge miR-655-3p, which targeted ACER3. Besides that, miR-655-3p silencing abolished the anticancer action of circ_0001955 silencing on HCC cells. Moreover, miR-655-3p overexpression inhibited HCC cell oncogenic phenotypes mentioned above, which were attenuated by ACER3 up-regulation. Additionally, circ_0001955 knockdown also impeded HCC growth in a mouse model. In all, this study suggested a novel circ_0001955/miR-655-3p/ACER3 pathway in HCC progression.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
ARN Neoplásico
/
Regulación Enzimológica de la Expresión Génica
/
Regulación Neoplásica de la Expresión Génica
/
Regulación hacia Arriba
/
Carcinoma Hepatocelular
/
MicroARNs
/
Ceramidasa Alcalina
/
Carcinogénesis
/
Neoplasias Hepáticas
/
Proteínas de Neoplasias
Límite:
Humans
Idioma:
En
Revista:
Bioengineered
Año:
2022
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Estados Unidos