Z-ajoene causes cell cycle arrest at G2/M and decrease of telomerase activity in HL-60 cells / 中华肿瘤杂志
Chinese Journal of Oncology
; (12): 516-520, 2005.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-358583
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the molecular mechanisms of Z-ajoene mitosis blocking and telomerase inhibitory effects on HL-60 cells.</p><p><b>METHODS</b>Proliferation inhibition of HL-60 cell line was evaluated by MTT assay. Z-ajoene-induced mitotic blocking effect was investigated by flow cytometry. Immunoblotting analysis was used to determine cell cycle regulatory proteins. The telomerase activity of HL-60 cells was detected by TRAP-silver stain assay. Telomerase hTRT and TP1 mRNA level were determined by RT-PCR.</p><p><b>RESULTS</b>Z-ajoene displayed great proliferation inhibiting effect on HL-60 cells. Progressive increase in the percentage of mitotic block at G(2)/M phase was observed from 4 h to 12 h after treatment with 10 micromol/L Z-ajoene, with a peak at 10 h, which was 1.95 times higher than that in control. Z-ajoene also caused an increase in cyclin B1 accumulation and a decrease of p34(cdc2) expression. But Z-ajoene did not change the level of cyclin A. After treating with 10 micromol/L Z-ajoene for 24 h, the telomerase activity of HL-60 cells was also decreased in a dose-independent manner. Furthermore, telomerase hTRT and TP1 mRNA levels decreased after 10 micromol/L Z-ajoene treatment for 24 h.</p><p><b>CONCLUSION</b>The results suggest that Z-ajoene has potent anti-cancer activity, and that its inhibitory effect on telomerase activity and on cell growth might be the result of G(2)/M phase blocking.</p>
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Ciclo Celular
/
Química
/
Telomerase
/
Células HL-60
/
Dissulfetos
/
Alho
/
Metabolismo
/
Mitose
/
Antineoplásicos Fitogênicos
Tipo de estudo:
Estudo de etiologia
Limite:
Humanos
Idioma:
Chinês
Revista:
Chinese Journal of Oncology
Ano de publicação:
2005
Tipo de documento:
Artigo