The flavonoid quercetin transiently inhibits the activity of taxol and nocodazole through interference with the cell cycle.
Nutr Cancer
; 62(8): 1025-35, 2010.
Article
em En
| MEDLINE
| ID: mdl-21058190
ABSTRACT
Quercetin is a flavonoid with anticancer properties. In this study, we examined the effects of quercetin on cell cycle, viability, and proliferation of cancer cells, either singly or in combination with the microtubule-targeting drugs taxol and nocodazole. Although quercetin induced cell death in a dose-dependent manner, 12.5-50 µM quercetin inhibited the activity of both taxol and nocodazole to induce G2/M arrest in various cell lines. Quercetin also partially restored drug-induced loss in viability of treated cells for up to 72 h. This antagonism of microtubule-targeting drugs was accompanied by a delay in cell cycle progression and inhibition of the buildup of cyclin-B1 at the microtubule organizing center of treated cells. However, quercetin did not inhibit the microtubule targeting of taxol or nocodazole. Despite the short-term protection of cells by quercetin, colony formation and clonogenicity of HCT116 cells were still suppressed by quercetin or quercetin-taxol combination. The status of cell adherence to growth matrix was critical in determining the sensitivity of HCT116 cells to quercetin. We conclude that although long-term exposure of cancer cells to quercetin may prevent cell proliferation and survival, the interference of quercetin with cell cycle progression diminishes the efficacy of microtubule-targeting drugs to arrest cells at G2/M.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Quercetina
/
Nocodazol
/
Ciclo Celular
/
Paclitaxel
/
Moduladores de Tubulina
/
Neoplasias
/
Antineoplásicos Fitogênicos
Limite:
Humans
Idioma:
En
Revista:
Nutr Cancer
Ano de publicação:
2010
Tipo de documento:
Article
País de afiliação:
Estados Unidos