Abstract
Dehydroepiandrosterone (DHEA) exerts opposite effects on the growth of mammary carcinoma. A stimulatory effect is observed in absence of estrogens, due to interaction of DHEA metabolite(s) with the estrogen receptor (ER); by contrast, in presence of estrogens DHEA inhibits tumor growth. The mechanism underlying the latter DHEA effect, which might be related to activation of the androgen receptor (AR), is poorly understood. Focusing on this point, we measured over a 20 days period the areas of DMBA-induced mammary tumors in rats given DHEA and/or the anti-androgen flutamide (FLU). Results show that DHEA inhibitory effect on the growth of mammary carcinoma is no longer observed when the ARs are blocked by FLU. Data are consistent with an involvement of ARs in the inhibitory effect of DHEA.
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