A GREB1-steroid receptor feedforward mechanism governs differential GREB1 action in endometrial function and endometriosis.

ABSTRACT: Cellular responses to the steroid hormones, estrogen (E2), and progesterone (P4) are governed by their cognate receptor's transcriptional output. However, the feed-forward mechanisms that shape cell-type-specific transcriptional fulcrums for steroid receptors are unidentified. Herein, we found that a common feed-forward mechanism between GREB1 and steroid receptors regulates the differential effect of GREB1 on steroid hormones in a physiological or pathological context. In physiological (receptive) endometrium, GREB1 controls P4-responses in uterine stroma, affecting endometrial receptivity and decidualization, while not affecting E2-mediated epithelial proliferation. Of mechanism, progesterone-induced GREB1 physically interacts with the progesterone receptor, acting as a cofactor in a pos

SUBMITTER: Chadchan SB 

PROVIDER: S-EPMC10908778 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature