Down-regulation of survivin in growth inhibition of hepatoma cells induced by a selective cyclooxygenase-2 inhibitor / 대한간학회지
The Korean Journal of Hepatology
; : 351-359, 2008.
Article
em Ko
| WPRIM
| ID: wpr-219567
Biblioteca responsável:
WPRO
ABSTRACT
BACKGROUND/AIMS: Cyclooxygenase-2 (COX-2) inhibitors reportedly inhibit the growth of hepatocellular carcinoma (HCC) via caspase-dependent or caspase-independent apoptosis, which is due to COX-2 being associated with hepatocarcinogenesis. Survivin is highly expressed in most human cancers, but the mechanism regulating survivin expression remains unclear. We investigated the regulatory expression of survivin in selective-COX-2-inhibitor-induced growth inhibition of hepatoma cells. METHODS: After treatment with NS-398 (a selective COX-2 inhibitor) at various concentrations (10, 50, 100, 150, and 200 micrometer), the growth inhibition of Hep3B hepatoma cells was assessed by an MTT cell-viability assay, DNA fragmentation gel analysis, and flow cytometry. The expression of survivin transcript was analyzed by reverse-transcription polymerase chain reactions. RESULTS: NS-398 inhibited the growth of hepatoma cells by an amount dependent on the concentration and the time since treatment. Apoptotic DNA ladder and flow-cytometry shifting to the sub-G1 phase were revealed in NS-398-induced growth inhibition of hepatoma cells. NS-398 suppressed the expression of the survivin gene in a concentration- and time-dependent manner. CONCLUSIONS: Survivin was down-regulated in the growth inhibition of hepatoma cells induced by a selective COX-2 inhibitor, NS-398, in a concentration- and time-dependent manner. These results suggest the therapeutic inhibition of COX-2 via suppression of survivin in HCC.
Palavras-chave
Texto completo:
1
Base de dados:
WPRIM
Assunto principal:
Sulfonamidas
/
Fatores de Tempo
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Fase G1
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Carcinoma Hepatocelular
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Reação em Cadeia da Polimerase Via Transcriptase Reversa
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Linhagem Celular Tumoral
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Proliferação de Células
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Inibidores de Ciclo-Oxigenase 2
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Neoplasias Hepáticas
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Proteínas Associadas aos Microtúbulos
Limite:
Humans
Idioma:
Ko
Revista:
The Korean Journal of Hepatology
Ano de publicação:
2008
Tipo de documento:
Article