Induction of cell cycle arrest and apoptosis in human breast cancer cells by quercetin.
- Authors
- Choi J.A.; Kim J.Y.; Lee J.Y.; Kang C.M.; Kwon H.J.; Yoo Y.D.; Kim T.W.; Lee Y.S.; Lee S.J.
- Issue Date
- 2001
- Citation
- International journal of oncology, v.19, no.4, pp 837 - 844
- Pages
- 8
- Indexed
- SCOPUS
- Journal Title
- International journal of oncology
- Volume
- 19
- Number
- 4
- Start Page
- 837
- End Page
- 844
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/22870
- ISSN
- 1019-6439
1791-2423
- Abstract
- Quercetin, a widely distributed bioflavonoid, has been shown to induce growth inhibition in certain cancer cell types. In the present study we have pursued the mechanism of growth inhibition in MCF-7 human breast cancer cells. Quercetin treatment resulted in the accumulation of cells specifically at G2/M phase of the cell cycle. Mitotic index measured by MPM2 staining clearly showed that cells were transiently accumulated in M phase, 24 h after treatment. The transient M phase accumulation was accompanied by a transient increase in the levels of cyclin B1 and Cdc2 kinase activity. However, 24 h or longer treatment caused a marked accumulation of cells in G2 instead of M phase. Levels of cyclin B1 and cyclin B1-associated Cdc2 kinase activity were also decreased. We also found that quercetin markedly increased Cdk-inhibitor p21CIP1/WAF1 protein level after treatment for 48 h or longer, and the induction of p21CIP1/WAF1 increased its association with Cdc2-cyclin B1 complex, however, up-regulation of p53 by quercetin was not observed. Quercetin also induced significant apoptosis in MCF-7 cells in addition to cell cycle arrest, and the induction of apoptosis was markedly blocked by antisense p21CIP1/WAF1 expression. The present data, therefore, demonstrate that a flavonoid quercetin induces growth inhibition in the human breast carcinoma cell line MCF-7 through at least two different mechanisms; by inhibiting cell cycle progression through transient M phase accumulation and subsequent G2 arrest, and by inducing apoptosis.
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Collections - 3. Graduate School > Biomedical Research Center > 1. Journal Articles
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