TGF-beta induced RBL2 expression in renal cancer cells by down-regulating miR-93
Clin. transl. oncol. (Print)
; 16(11): 986-992, nov. 2014.
Artigo
em Inglês
| IBECS
| ID: ibc-128640
Biblioteca responsável:
ES1.1
Localização: BNCS
ABSTRACT
PURPOSE:
TGF-beta can induce G1 arrest via many mechanisms including up-regulating p21, p27, and Rb. However, as the member of Rb family, whether RBL2 is induced by TGF-beta treatment remains exclusive.METHODS:
The expression of RBL2 and miR-93 after TGF-beta treatment was determined by quantitative real-time PCR and western blot. The growth of renal cancer cells was determined by CCK-8 assays and cell cycle was determined by PI staining. The binding of miR-93 on RBL2 3'-UTR was determined by double luciferase system.RESULTS:
In renal cancer cells, TGF-beta treatment induced expression of RBL2 in a time- and concentration-dependent manner, and RBL2 mediated TGF-beta induced growth inhibition and cell cycle arrest in renal cancer cells. Furthermore, we found that miR-93 directly targeted RBL2 by binding to its 3'-UTR in renal cancer cells. Over-expression of miR-93 significantly reduced the expression of RBL2, whereas knock down of miR-93 up-regulated the expression of RBL2. More importantly, TGF-beta treatment inhibited miR-93 expression, which resulted in up-regulation of RBL2 after TGF-beta treatment.CONCLUSION:
TGF-beta induced RBL2 expression through down-regulating miR-93 in renal cancer cells. The newly identified TGF-beta/miR-93/RBL2 signal pathway reveals a new mechanism of TGF-beta induced growth arrest in renal cancer (AU)RESUMEN
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Espanha
Base de dados:
IBECS
Assunto principal:
Fator de Crescimento Transformador beta
/
Neoplasias Renais
Tipo de estudo:
Estudo prognóstico
Limite:
Humanos
Idioma:
Inglês
Revista:
Clin. transl. oncol. (Print)
Ano de publicação:
2014
Tipo de documento:
Artigo
Instituição/País de afiliação:
China Medical University/China
/
Hebei Medical University/China