RESUMO
The influence of 17beta-estradiol (E2), tamoxifen (TAM) and raloxifen (RLX) on the proliferation of breast (BC) and endometrial carcinoma cell lines (EC) and the expression of different compounds of the estrogen receptor (ER)-transactivation machinery were studied. E2 stimulated the proliferation of BC, but had no effect on the EC. TAM showed a biphasic effect on ER-positive cell lines. RLX showed an antagonistic suppression or no effect. The expression of ERalpha was down-regulated by E2, but not affected by selective estrogen receptor modulators. ERbeta and progesterone receptor expressions were up-regulated by E2, TAM and OHT. This supports the hypothesis that ERbeta expression is also regulated via the ERalpha-pathway. The steroid receptor coactivator (SRC) AIB1 expression was slightly decreased by E2 but not by antiestrogens (antiE). TIF2 expression was increased by E2, TAM and RLX, but SRC-1 expression was not. In comparison, the expressions of ERbeta and progesterone receptor were strongly influenced by antiE, while the expression of SRCs was only slightly affected.
