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Original Article
- Genistein Induced Inginition of Cell Proliferation and Programmed Cell Death in the Human Cancer Cell Lines
- Young Hyun Choi, Soo Jae Lee, Min Kim, Lijuan Zhang, Won Ho Lee, Kun Young Park
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Journal of the Korean Cancer Association 1998;30(4): 800-808.
1National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
2Korea Cancer Center Hospital, Seoul, Korea.
3epartment of Biology, Pusan National University, Pusan, Korea.
4Department of Food Science & Nutrition and Pusan Cancer Research Center, Pusan National University, Pusan, Korea.
2Korea Cancer Center Hospital, Seoul, Korea.
3epartment of Biology, Pusan National University, Pusan, Korea.
4Department of Food Science & Nutrition and Pusan Cancer Research Center, Pusan National University, Pusan, Korea.
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Abstract
PURPOSE
Genistein, a natural isoflavonoid phyto-oestrogen present in plant foods including citrus fruits and soybean, is a specific inhibitor of tyrosine kinase and topoisomerase II. In this paper we examined the effect of genistein on cell cycle progression and programmed cell death in the human prostate carcinoma PC-3 and Ewing's sarcoma CHP-100 cells.
MATERIAL AND METHODS: Effect of genistein on cell cycle was measured by DNA flow cytometric analysis. In order to understand anticancer effect of genistein on cell cycle, Western blot analysis, immune complex kinase assay, DAPI staining and DNA fragmentation analysis were conducted.
RESULTS
DNA flow cytometric analysis indicated that genistein induced cell cycle arrest at the G2/M transition phase. Western blot analyses showed that genistein selectively reduced expression of cyclin B1 and cdk2-dependent kinase activity in both cell lines. Genistein also induced apoptosis that was demonstrated by direct visualization of morphological nuclear changes and confirmed by the production of characteristic ladder patterns of genomic DNA fragmentation.
CONCLUSION
The chemopreventive activity of genistein is proven to be related with the induction of cell cycle arrest at the G2/M transition phase by reducing the expression of cyclin B1 and cdk2-dependent kinase activity, and also with the induction of apoptosis in the tested cancer cells.
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