Estrogen-modulated estrogen receptor pit-1 protein complex formation and prolactin gene activation require novel protein synthesis

Authors
Citation
Cw. Ying et Dh. Lin, Estrogen-modulated estrogen receptor pit-1 protein complex formation and prolactin gene activation require novel protein synthesis, J BIOL CHEM, 275(20), 2000, pp. 15407-15412
Citations number
46
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Biochemistry & Biophysics
Journal title
JOURNAL OF BIOLOGICAL CHEMISTRY
ISSN journal
0021-9258 → ACNP
Volume
275
Issue
20
Year of publication
2000
Pages
15407 - 15412
Database
ISI
SICI code
0021-9258(20000519)275:20<15407:EERPPC>2.0.ZU;2-E
Abstract
Both estrogen receptor (ER) and Pit-1 proteins are essential for the estrog en-activated expression of the rat prolactin gene. Our results show that ER Pit-1 protein complex formation is reduced by estrogen in GH3 and PR1 rat pituitary tumor cells. In the latter, this decrease was blocked by cyclohex imide, a protein synthesis inhibitor. On the other hand, the direct additio n of estrogen to PR1 cell lysates had no effect on the formation of ER Pit- 1 complexes. Estrogen-activated prolactin gene expression was also inhibite d by cycloheximide, suggesting that some form of protein synthesis is invol ved in ER Pit-1 complex formation and subsequent prolactin gene activation. In support of this notion, we showed that estrogen-induced regulation of E R Pit-1 complex formation could be transferred from cell lysates prepared f rom estrogen-treated PR1 cells to control cell lysates. This is not true fo r GH3 cells; instead, direct administration of estrogen to GH3 cell lysates readily abolished ER Pit-1 protein complex formation in a dose-dependent m anner, and such estrogen-induced regulation was blocked by the antiestrogen ICI 182,780, These findings thus indicate that 1) interaction between ER a nd Pit-1 proteins is estrogen-regulated in ways specific to different cell types, and 2) auxiliary protein factor synthesis may be involved in this pr ocess.