BACKGROUND: Estrogens and polyamines seem to play an important role not only in cell growth and differentiation, but also in programmed cell death. The aim of the present study was to investigate the effects of 17beta-estradiol supplementation on apoptosis as well as on the polyamine content of an ER-positive human gastric cancer cell line (AGS). MATERIALS AND METHODS: Apoptosis was investigated by evaluating DNA fragmentation, using enzyme immunoassay and agarose gel electrophoresis and the phosphatidylserine exposure by flow cytometry analysis. Polyamine levels were evaluated by HPLC. RESULTS: 17Beta-estradiol gave rise to a marked pro-apoptotic effect at concentrations of 16 microM or higher compared to the control. Moreover, the hormone significantly reduced the contents of polyamines compared to control cells. The apoptotic effect of 17beta-estradiol was partially counteracted by exogenous spermine administration. CONCLUSION: 17Beta-estradiol administration induces apoptosis in AGS cells. Further, an increase in cell sensitivity to apoptosis due to a decline in the polyamine content may be suggested.
BACKGROUND: Estrogens and polyamines seem to play an important role not only in cell growth and differentiation, but also in programmed cell death. The aim of the present study was to investigate the effects of 17beta-estradiol supplementation on apoptosis as well as on the polyamine content of an ER-positive humangastric cancer cell line (AGS). MATERIALS AND METHODS: Apoptosis was investigated by evaluating DNA fragmentation, using enzyme immunoassay and agarose gel electrophoresis and the phosphatidylserine exposure by flow cytometry analysis. Polyamine levels were evaluated by HPLC. RESULTS:17Beta-estradiol gave rise to a marked pro-apoptotic effect at concentrations of 16 microM or higher compared to the control. Moreover, the hormone significantly reduced the contents of polyamines compared to control cells. The apoptotic effect of 17beta-estradiol was partially counteracted by exogenous spermine administration. CONCLUSION:17Beta-estradiol administration induces apoptosis in AGS cells. Further, an increase in cell sensitivity to apoptosis due to a decline in the polyamine content may be suggested.
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