We tested the effects of 17β-estradiol as well as its catechol- and methoxy-derivatives,
two androgens (DHEA and testosterone), a glucocorticoid (cortisol), a mineralocorticoid
(aldosterone), and progesterone on the activity of ERK1,2 , a key component of the ERK/MAPK enzyme phosphorylation cascade, in SW-13 human adrenal
carcinoma cells. After a 24-hour exposure SW-13 cells incubated with 10-5 M concentrations of 17β-estradiol, its 2-hydroxy or its 2-methoxy derivative, all
had elevated ERK activities (196 %, 159 %, and 275 %, respectively) relative to control
cells (p < 0.01). Incubation with testosterone resulted in 162 % of control ERK activity
(p < 0.01), whereas incubation with the far weaker androgen DHEA or with cortisol,
aldosterone, or progesterone had no significant effects. These findings suggest sex
steroid-specific influences in the induction or activation of signal transduction
pathways known to play a crucial role in cellular proliferation and differentiation.
Key words:
Adrenal Carcinoma - Steroids - MAPK - ERK
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1 This work was supported by the U.S. Department of Veterans Affairs.
Dr. J. W. Brown
Adrenal Research (151) V.A. Medical Center
1201 N.W. 16 St. Miami, FL 33125 U.S.A.
Telefon: Phone:+ 1 (305) 324-3195
Fax: Fax:+ 1 (305) 324-3126