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SECOND INTERNATIONAL SYMPOSIUM
ON THE ROLE OF SOY
IN PREVENTING AND TREATING CHRONIC DISEASESeptember 15-18, 1996
Brussells, Belgium
POSTER ABSTRACTSDIFFERENTIAL EFFECTS OF GENISTEIN AND DAIDZEIN ON GROWTH OF HUMAN COLON CANCER CELL LINES
L. D. Bourquin and M. R. Bennink
Michigan State University, East Lansing, MI 48824 USA
A series of experiments was conducted to determine the effects of genistein and daidzein on the growth of human colon cancer cells in culture. Two cell lines, HCT 116 and HT-29, were used in all experiments and were cultured in a base medium of 90% McCoy's 5A Medium:10% fetal bovine serum. In experiment 1, the effects of isoflavone concentrations ranging from 0 to 80 (M were tested. The concentration of genistein required to cause a 50% inhibition of cell growth (IC50) was approximately 15 (M for HCT 116 cells and 50 (M for HT-29 cells. The daidzein IC50 was approximately 80 (M for HCT 116 cells, but was not reached for HT-29 cells. In experiment 2, isoflavones were administered to cell lines both singly and in combination. Results indicated that inhibition of cell growth by genistein and daidzein was additive. The effects of intermittent (6 hr/day) versus continuous exposure of cell lines to isoflavones was tested in experiment 3. Intermittent exposure of cell lines to isoflavones resulted in a considerable attenuation of the growth-inhibitory effects of isoflavones, indicating that these effects are transient. Cell cycle analysis of HCT 116 cells indicated that genistein caused an accumulation of cells in G2-M, whereas daidzein caused an accumulation in G1 phase. Cell cycle distribution of HT-29 cells was only minimally affected by isoflavones, even when administered at large concentrations. A final experiment was conducted to determine if the isoflavone glycosides, genistin and daidzin, had any effect on colon cancer cell growth. Initial observations indicated that glycosides were as effective as aglycones in inhibiting cell growth. However, analysis of culture media at the end of the experiment indicated that the isoflavone glycosides had been completely degraded to the aglycone forms. Interestingly, it was also observed that HT-29 cells conjugated isoflavone aglycones with glucuronide and/or sulfate, whereas HCT 116 cells did not conduct phase 2 metabolism on isoflavones. This observation probably explains why HT-29 cells were less susceptible to isoflavones than were HCT 116 cells, and also suggests that conjugated isoflavones probably are not biologically active.
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