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miR-149 inhibition of cell growth and invasion by targeting FOXM1 in human prostate carcinoma / 中国肿瘤临床
Chinese Journal of Clinical Oncology ; (24): 1080-1083, 2014.
Artigo em Chinês | WPRIM | ID: wpr-456687
ABSTRACT

Objective:

To investigate the effects of the miR-149 on the growth and invasion of prostate carcinoma cells. Meth-odsReal-time fluorescence quantitative polymerase chain reaction was performed to detect the expression of miR-149 on prostate car-cinoma tissues and paraneoplastic tissues. The PC3 and DU145 cells were transfected with miR-149 mimics and negative controls. The cell growth and invasion abilities were tested in terms of colony formation and via Transwell invasion assay. The cells were transfected with the siRNA of the target gene FOXM1 and siRNA control. Western blot was used to detect the expression of FOXM1. The cell colo-ny formation and invasion ability were also detected.

Results:

Compared with the paraneoplastic tissues, miR-149 was down-regulated in the prostate carcinoma tissues (P<0.01), and the FOXM1 mRNA was highly expressed (P<0.01). PC3 and DU145 cells with miR-149 mimics had only a few colonies and invading cells (P<0.01). Moreover, PC3 (P<0.01) and DU145 (P<0.05) with miR-149 mimics had a low protein level of FOXM1. The FOXM1 expression was knocked down by the siRNA of FOXM1 in the PC3 and the DU145 cells (P<0.01). The knocking down of FOXM1 resulted in an inhibition of the cell colony formation and invasion abilities (P<0.01).

Conclusion:

The miR-149 inhibits prostate carcinoma cell growth and invasion by suppressing the FOXM1. Our data suggest that miR-149 may function as an effective tool for the molecular treatment of prostate cancer.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Clinical Oncology Ano de publicação: 2014 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Clinical Oncology Ano de publicação: 2014 Tipo de documento: Artigo