Cross talk between peptide growth factor and estrogen receptor signaling systems.

摘要: Abstract Epidermal growth factor reproduces many of the effects estrogen on murine female reproductive tract and may partially mediate estrogen-induced differentiation. The mechanism by which actions estrogens epidermal (EGF) converge is unknown. studies described herein were performed to investigate possibility that some EGF be mediated through receptor. A specific receptor (ER) antagonist inhibited estrogenlike in mouse uterus, specifically induction DNA synthesis phosphatidylinositol turnover. In addition, elicited enhanced nuclear localization uterine ER formation a unique form present after treatment. These vivo observations indicated elicit its activation ER. Thus, effect peptide factors consensus response element was assessed Ishikawa human endometrial adenocarcinoma cells, contain negligible levels, BG-1 ovarian abundant TGF alpha induced transcriptional (ERE) an ER-dependent manner both cell types. insulinlike I (IGF-I) as potent 17 beta-estradiol cells. Synergism between observed types, although synergism not different classes [i.e., transforming (TGF alpha) IGF-I] most activator ERE-dependent transcription protein kinase C (TPA), acted synergistically with beta-estradiol. inhibitor abolished TPA but beta-estradiol, IGF-I, or alpha. did synergize factors. conclusion, physiologic are dependent Indeed, capable eliciting ERE. Both pathways can activation; however, it unlikely these