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Nutr Cancer. 2010;62(8):1025-35. doi: 10.1080/01635581.2010.492087.

The flavonoid quercetin transiently inhibits the activity of taxol and nocodazole through interference with the cell cycle.

Author information

1
Pathobiology Department, Tuskegee University, College of Veterinary Medicine, Nursing and Allied Health, Tuskegee, Alabama 36088, USA. tsamuel@tuskegee.edu

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.

PMID:
21058190
PMCID:
PMC3021775
DOI:
10.1080/01635581.2010.492087
[Indexed for MEDLINE]
Free PMC Article

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