한빛사 논문
J-W Jeong1, HS Lee2, HL Franco1, RR Broaddus3, MM Taketo4, SY Tsai1, JP Lydon1 and FJ DeMayo1,*
1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA;
2Infertility & Reproductive Endocrinology Center, Department of Obstetrics and Gynecology, MizMedi Hospital, Seoul, Korea;
3Department of Pathology, University of Texas M.D. Anderson Cancer Center, Houston, TX, USA
4Department of Pharmacology, Graduate School of Medicine, Kyoto University, Yoshida-Konoe´-cho, Sakyo, Kyoto, Japan
*Corresponding author
Abstract
Endometrioid adenocarcinoma is the most frequent form of endometrial cancer, usually developing in pre- and peri-menopausal women. β-catenin abnormalities are common in endometrioid type endometrial carcinomas with squamous differentiation. To investigate the role of β-catenin (Ctnnb1) in uterine development and tumorigenesis, mice were generated which expressed a dominant stabilized β-catenin or had β-catenin conditionally ablated in the uterus by crossing the PRCre mouse with the Ctnnb1f(ex3)/+ mouse or Ctnnb1f/f mouse, respectively. Both of the β-catenin mutant mice have fertility defects and the ability of the uterus to undergo a hormonally induced decidual reaction was lost. Expression of the dominant stabilized β-catenin, PRcre/+Ctnnb1f(ex3)/+, resulted in endometrial glandular hyperplasia, whereas ablation of β-catenin, PRcre/+Ctnnb1f/f, induced squamous cell metaplasia in the murine uterus. Therefore, we have demonstrated that correct regulation of β-catenin is important for uterine function as well as in the regulation of endometrial epithelial differentiation.
논문정보
관련 링크
관련분야 연구자보기
소속기관 논문보기
관련분야 논문보기
해당논문 저자보기