Silencing of lncRNA UCA1 curbs proliferation and accelerates apoptosis by repressing SIRT1 signals by targeting miR-204 in pediatric AML.
J Biochem Mol Toxicol
; 34(3): e22435, 2020 Mar.
Article
en En
| MEDLINE
| ID: mdl-31916649
ABSTRACT
The long noncoding RNA urothelial carcinoma-associated 1 (UCA1) has been reported to sustain the proliferation of acute myeloid leukemia (AML) cells through downregulating cell cycle regulators p27kip1 . Yet, the foundational mechanism of UCA1 in AML pathologies remains unclear. Herein, we found an escalation of UCA1 expression and suppression of miR-204 expression in pediatric AML patients and cells. UCA1 silencing suppressed cell proliferative abilities, promoted apoptotic rates, decreased Ki67, and increased cleaved caspase-3 in AML cells. Moreover, UCA1 sponged miR-204 and suppressed its expression. UCA1 overexpression inversed the miR-204 suppressed proliferation and promoted apoptosis. UCA1 also boosted the expression of SIRT1, a miR-204 target, via the sponging interaction. Furthermore, miR-204 inhibited inducible nitric oxide synthase and cyclooxygenase-2 expression, while UCA1 overexpression inversed the inhibitory effects in AML cells. Our findings concluded that UCA1 downregulation repressed cell proliferation and promoted apoptosis through inactivating SIRT1 signals by upregulating miR-204 in pediatric AML.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
ARN Neoplásico
/
Leucemia Mieloide Aguda
/
Apoptosis
/
Silenciador del Gen
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MicroARNs
/
Proliferación Celular
/
Sirtuina 1
/
ARN Largo no Codificante
/
Proteínas de Neoplasias
Límite:
Child
/
Female
/
Humans
/
Male
Idioma:
En
Año:
2020
Tipo del documento:
Article