Diethylstilbestrol (DES) is used in the treatment of menopausal and postmenopausal disorders.

Diethylstilbestrol promotes coactivator release from orphan nuclear receptor ERR beta and inhibits its transcriptional activity in trophoblast stem cells. [1]

Diethylstilbestrol treated pregnant mice exhibits abnormal early placenta development associated with an overabundance of trophoblast giant cells and an absence of diploid trophoblast. [1] Diethylstilbestrol causes epigenetic methylation changes that result in persistent alterations in gene expression, leading to tumorigenesis in mouse uterus. Diethylstilbestrol induces c-fos exon-4 hypomethylation at postnatal day 17 in mice uterus, while elevating its mRNA level from postnatal day 5. Diethylstilbestrol exposure leads to hypomethylation in the exon-4 region of c-fos mRNA. [2] Diethylstilbestrol-treated rats exhibits more pronounced delay in maturational development of an adult pattern of immunoexpression of the three proteins compared with GnRHa-treated rats. Diethylstilbestrol results in similar reductions in both Sertoli cell numbers and suppression of testicular growth at 18 and 25 days, though by 35 days the suppression is more pronounced in DES-treated rats. [3] Diethylstilbestrol treatment appears to imprint an abnormal, site-specific demethylation of CpG/-464, which requires ovarian hormones to occur in adult mice. [4] Diethylstilbestrol (2.0 ng/g) per day increases adult prostate weight, whereas a 200 ng/g dose decreases adult prostate weight in male offspring mice. [5]