MIG-6 suppresses endometrial epithelial cell proliferation by inhibiting phospho-AKT.

ABSTRACT:

Background

Aberrant hyperactivation of epithelial proliferation, AKT signaling, and association with unopposed estrogen (E2) exposure is the most common endometrial cancer dysfunction. In the normal uterus, progesterone (P4) inhibits proliferation by coordinating stromal-epithelial cross-talk, which we previously showed is mediated by the function of Mitogen-inducible gene 6 (Mig-6). Despite their attractive characteristics, non-surgical conservative therapies based on progesterone alone have not been universally successful. One barrier to this success has been the lack of understanding of the P4 effect on endometrial cells.

Method

To further understand the role of Mig-6 and P4 in controlling uterine proliferation, we developed a Sprr2f-cre driven mouse model where Mig-6 is

SUBMITTER: Yoo JY 

PROVIDER: S-EPMC5975686 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature