Mechanism of lithium chloride-induced proliferation inhibition and apoptosis of K562 leukemic cells / 中国实验血液学杂志
Journal of Experimental Hematology
; (6): 979-982, 2005.
Article
em Zh
| WPRIM
| ID: wpr-343844
Biblioteca responsável:
WPRO
ABSTRACT
To investigate the mechanism of proliferation inhibition and apoptosis of K562 leukemia cells by lithium chloride (LiCl), after K562 cells were treated with LiCl (30 mmol/L) cell cycle was examined by flow cytometry (FCM) and the expression of bcr/abl fusion gene mRNA was evaluated by RT-PCR. The intracellular Li(+) concentrations of K562 cells were determined at different time after treated with 30 mmol/L LiCl and the effects of TTX and FSK on intracellular Li(+) concentrations of K562 cells were also detected by atomic absorption spectrometry. The effects of TTX and FSK on LiCl-induced growth inhibition of K562 cells were determined by cell counting in liquid culture. The results showed that LiCl (30 mmol/L) caused a sustained arrest in G(2)/M cell cycle and down-regulated the bcr/abl mRNA expression in K562 cells, the intracellular Li(+) concentration of K562 cells increased at 30 minutes after treated with 30 mmol/L LiCl and reached apex at 2 hours, thereafter, gradually decreased and balanced at 4 hours after the treatment. If either Na(+) channel was pre-blocked with TTX or K(+) channel was pre-blocked with FSK, the intracellular Li(+) concentrations of K562 cells treated with 30 mmol/L LiCl were higher than that in the cells just treated with LiCl without pre-blocking. Furthermore, after pre-blocking either Na(+) channel with TTX or K(+) channel with FSK, the inhibition rate of K562 cell growth by 30 mmol/L LiCl could be increased. It is concluded that the mechanism of proliferation inhibition and apoptosis of K562 leukemia cells induced by LiCl is probably related with the G(2)/M cell cycle arrest, the bcr/abl mRNA expression down-regulation and the status of Na(+), K(+), or Li(+) ion channels on K562 leukemia cells.
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Base de dados:
WPRIM
Assunto principal:
Patologia
/
Farmacologia
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Tetrodotoxina
/
Colforsina
/
RNA Mensageiro
/
Leucemia
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Regulação Neoplásica da Expressão Gênica
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Ciclo Celular
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Proteínas de Fusão bcr-abl
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Apoptose
Limite:
Humans
Idioma:
Zh
Revista:
Journal of Experimental Hematology
Ano de publicação:
2005
Tipo de documento:
Article