Genistein Induced Inginition of Cell Proliferation and Programmed Cell Death in the Human Cancer Cell Lines.
- Author:
Young Hyun CHOI
1
;
Soo Jae LEE
;
Min KIM
;
Lijuan ZHANG
;
Won Ho LEE
;
Kun Young PARK
Author Information
1. National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
- Publication Type:Original Article
- Keywords:
Genistein;
Cancer cells;
Cell cycle arrest;
Apoptosis
- MeSH:
Antigen-Antibody Complex;
Apoptosis;
Blotting, Western;
Cell Cycle;
Cell Cycle Checkpoints;
Cell Death*;
Cell Line*;
Cell Proliferation*;
Citrus;
Cyclin B1;
DNA;
DNA Fragmentation;
DNA Topoisomerases, Type II;
Genistein*;
Humans*;
Phosphotransferases;
Plants;
Prostate;
Protein-Tyrosine Kinases;
Sarcoma, Ewing;
Soybeans
- From:Journal of the Korean Cancer Association
1998;30(4):800-808
- CountryRepublic of Korea
- Language:Korean
-
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.
