INDUCTION OF APOPTOSIS IN OVARIAN-CARCINOMA CELL-LINE BY GLUCOCORTICOIDS, AND SEX STEROID-HORMONES

We investigated the interactions in the KOC-2s human ovarian cancer ce lls on the effect of glucocorticoids, and sex steroid hormones in ovar ian carcinomas. At 10(-8) M to 10(-5) M, dexamethasone (Dex) decreased the number of cells by 75-80% (p<0.001). At 10(-8) M and 10(-7) M, hy drocortisone (HC) decreased the number by 50% (p<0.01); at 10(-6) M an d 10(-5) M, the decrease in number of cells was 65%. The E-2 decrease in number was not statistically significant. Progesterone (PG) showed at 10(-8) to 10(-6) M an increase in number of cells, however, at 10(- 5) M it was decreased by 70% with a significant difference (p<0.001). Dex (10(-8)-10(-5) M), HC (10(-8)-10(-5) M) and PG (10(-5) M) produced internucleosomal cleavage of DNA into fragments with multiples of 180 to 200 bp. The TNF-alpha with addition of Dex (10(-8)-10(-5) M) and H C (10(-8)-10(-5) M) was increased after 24 h, 48 h (p<0.001); however, gradually decrease after 72 h. When PG (10(-8)-10(-5) M) was added, P G (10(-5) M) increased the secretion of TNF-alpha after 72 h. Our find ings demonstrate that glucocorticoids, and PG directly induce apoptoti c DNA fragmentation of KOC-2s cells. However, the secretion of TNF-alp ha and expression of Fas antigen were totally different in these subst ances. These data provide a basis for future studies on the mechanisms of apoptotic effect of glucocorticoids, and PG and the therapeutic ef fects of these substances.