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It is well known that estrogen (E2) induces progesterone receptor (PR) in the uterus and the mammary gland. In MtT/F84, a pituitary tumor, which was established in our laboratory and has been maintained with in vivo passages, we investigated the PR regulation by E2 in relation to the host's thyroidal status. The PR level in the tumor had increased five fold 48 h after an E2 injection. When the host rats were treated with propylthiouracil (PTU), an anti-thyroid drug, the induction of PR after an E2 injection was completely blocked. This result is consistent with our previous findings indicating that E2 responsiveness in the tumor may be under the control of thyroid hormones. The estrogen receptor (ER) level in the tumor treated with PTU was 15% of the control. This low ER level may account for the blocking of PR induction after an E2 injection. When the host animals were continuously treated with various doses of E2, the PR level in the tumor rose in correlation with the E2 doses. PTU administration, however, did not prevent long term induction of PR by continuous E2 treatment. Our findings suggest that PTU lower the ER level and suppresses the short term estrogenic actions such as PR induction after an E2 injection.

endocrine journal

Blockade of the Estrogen Induced Increase in Progesterone Receptor Caused by Propylthiouracil, an Anti-Thyroid Drug, in a Transplantable Pituihry Tumor in Rats.