Estradiol (E2) is the major molecular form of estrogens. Its biological effects are determined by estrogen receptors and intracellular E2 concentration in target cells. Regulation of intracellular E2 concentration involves the action of 17p-hydroxysteroid dehydrogenase (17HSD) type 2, the enzyme inactivating E2 to estrone. It has been demon-strated that 17HSD type 2 is expressed in normal endo-metrial epithelia and emdometrial carcinoma cells (RL 95-2). However, the regulatory mechanism of 17HSD type 2 expression in emdometrial cancer cells remains unknown. In the present study, the effects of transforming growth factor-β1 (TGF-β1) and epidermal growth factor (EGF) on 17HSD type 2 expression in RL 95-2 cells have been investigated using enzyme activity assay and Northern blot analysis. After stimulation with TGF-P1 or EGF, the in vivo oxidative 17HSD activity in RL 95-2 cells was significantly decreased. It appeared that the inhibitory effect of TGF-β1 and EGF onthe enzyme activity of 17HSD type 2 is Its biological effects are determined by estrogen receptors and intracellular E2 concentration in target cells. Regulation of intracellular E2 concentration involves the action of 17p-hydroxysteroid dehydrogenase (17HSD) type 2, the enzyme inactivating E2 to estrone. It has been demon-strated that 17 HSD type 2 is expressed in normal endo-metrial epithelia and emdometrial carcinoma cells (RL 95-2). However, the regulatory mechanism of 17 HSD type 2 expression in emdometrial cancer cells remains unknown. In the present study, the effects of transforming growth factor-β1 (TGF-β1) and epidermal growth factor (EGF) on 17HSD type 2 expression in RL 95-2 cells have been investigated using an enzyme activity assay and Northern blot analysis. with TGF-P1 or EGF, the in vivo oxidative 17 HSD activity in RL 95-2 cells was significantly decreased. It has that the inhibitory effect of TGF-β1 and EGF on the enzyme activity of 17HSD type 2 is