Effects of antisense Bmi-1 RNA on the proliferation of lung cancer cell line A549 / 中华病理学杂志
Chinese Journal of Pathology
;
(12): 829-832, 2009.
Artigo
em Chinês
| WPRIM
| ID: wpr-273467
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of antisense Bmi-1 (B cell-specific moloney murine leukemia virus insertion site 1) RNA on the growth, cell cycle and apoptosis of lung cancer cell line A549.</p><p><b>METHODS</b>Recombinant plasmids carrying antisense Bmi-1 RNA were transfected into A549 cells, which expressed a high level of endogenous Bmi-1. The mRNA level of A549 cell was analyzed by real time quantitative RT-PCR and the protein level was determined using Western blot. MTT growth curve and plate colony forming assay were used to measure the effect of antisense Bmi-1 RNA expression on the growth of A549. Flow cytometry was used to analyze cell cycle and apoptosis.</p><p><b>RESULTS</b>Antisense Bmi-1 RNA reduced the Bmi-1 expression at the protein level, but did not alter the mRNA level in A549 cells. Compared with the control cells, A549 cells transfected with antisense Bmi-1 RNA showed a strong inhibition of the cell growth. The number of plate colony formation of the antisense Bmi-1 transfected cells (0.67 +/- 0.50) was less than those of the control (73.0 +/- 4.1) and cells transfected with empty vector (67.0 +/- 4.0, P < 0.01). Transfection of antisense Bmi-1 RNA arrested the A549 cells at G₀/G₁ phase of the cell cycle and did not increase the apoptosis.</p><p><b>CONCLUSION</b>Antisense Bmi-1 RNA expression inhibits A549 cells proliferation, likely through the interference of Bmi-1 leading to an arrest of the proliferating cells at the G₀/G₁ phase.</p>
Texto completo:
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Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Farmacologia
/
Proteínas Repressoras
/
Proteínas Recombinantes
/
RNA Mensageiro
/
Proteínas Nucleares
/
Transfecção
/
Regulação para Baixo
/
Regulação Neoplásica da Expressão Gênica
/
Ciclo Celular
Limite:
Humanos
Idioma:
Chinês
Revista:
Chinese Journal of Pathology
Ano de publicação:
2009
Tipo de documento:
Artigo
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