RESEARCH: Normal endometrial function requires a balance of progesterone (P4) and estrogen (E2) effects. An imbalance caused by increased E2 action and/or decreased P4 action can result in abnormal endometrial proliferation and, ultimately, endometrial adenocarcinoma, the fourth most common cancer in women. Jeong‚Äôs laboratory has special interests in research relating to women's health, particularly infertility and cancer using genetically engineered mouse models.. We have identified mitogen-inducible gene 6 (Mig-6) as a down stream target of progesterone receptor (PR) and steroid receptor coactivator (SRC-1) action in the uterus. Mig-6 plays a critical role in the regulation of uterine function and the development of endometrial hyperplasia and cancer in the presence of steroid hormones. Importantly, the observation that endometrial carcinomas from women have a significant reduction in MIG-6 expression provides compelling support for an important growth regulatory role for Mig-6 in the uterus of both humans and mice. This demonstrates that Mig-6 is a critical regulator of the response of the endometrium to steroid hormones in regulating tissue homeostasis. Furthermore, this identifies a PR/SRC-1/Mig-6 regulatory pathway that is critical for the suppression of endometrial cancer. Current studies are aimed at the application of these genetic model systems to further study and understand the role of steroid hormone in women cancers, with the ultimate goal of developing therapies effective against tumors. These studies have broader implications for clinical application because of the benefits of animal models of translational research in women cancer.
Chang, Hye Jin
Kim, Tae Hoon, PhD
Tae Hoon Kim received his BS degree in chemistry and his Ph.D. degree in pharmacology from Chung-Ang University in Seoul, Korea. His research focuses on the role of Mig-6 in pregnancy, steroid hormone regulation and endometrial cancer using transgenic mice.