The analysis of molecular mechanism of the precipitation/inhibition of uterine endometrial epithelial cell proliferation by SERM

克罗米芬（CC）被认为是一种选择性雌激素受体调节剂（SERM），已被用于无排卵性不孕妇女。CC虽然能使80%左右的无排卵妇女恢复排卵，但只有20~ 30%的妇女妊娠。排卵成功率和妊娠成功率之间的这种差异可以通过CC在子宫内膜水平的外周抗雌激素作用来解释。然而，CC抑制子宫内膜细胞增殖的分子机制尚不清楚。探讨CC抑制雌激素（E2）诱导的子宫内膜上皮细胞增殖的分子机制，CC可能通过抑制SRC-1向ERα的募集来抑制E2诱导的子宫内膜上皮细胞增殖和ERα反式激活。

Clomiphene citrate (CC), which has been used for anovulatory infertile women, is thought to be a selective estrogen receptor modulator (SERM). Although CC will restore ovulation in about 80% of anovulatory women, it will result in pregnancy in only about 20~30%. This discrepancy between ovulation and pregnancy success rates may be explained by the peripheral anti-estrogenic effects of CC at the level of the endometrium. However, the molecular mechanisms how CC acts to inhibit the endometrial cell proliferation are still remains to be elusive. We investigated the molecular mechanisms by which CC inhibits the estrogen (E2)-induced endometrial epithelial cell proliferation and CC may inhibit the E2-induced endometrial epithelial cell proliferation and ERα transactivation through inhibiting the recruitment of SRC-1 to ERα.