Journal
ONCOGENE
Volume 28, Issue 1, Pages 31-40Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2008.363
Keywords
beta-catenin; uterus; estrogen; hyperplasia
Funding
- NICHD
- NIH [R01HD042311, U54HD0077495, R01- CA77530, 1P50CA098258-01, R01HD057873]
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Endometrioid adenocarcinoma is the most frequent form of endometrial cancer, usually developing in pre- and perimenopausal women. beta-catenin abnormalities are common in endometrioid type endometrial carcinomas with squamous differentiation. To investigate the role of beta-catenin (Ctnnb1) in uterine development and tumorigenesis, mice were generated which expressed a dominant stabilized beta-catenin or had beta-catenin conditionally ablated in the uterus by crossing the PRCre mouse with the Ctnnb1(f(ex3)/+) mouse or Ctnnb1(f/f) mouse, respectively. Both of the beta-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 beta-catenin, PR(cre/+)Ctnnb1(f(ex3)/+), resulted in endometrial glandular hyperplasia, whereas ablation of b-catenin, PR(cre/+)Ctnnb1(f/f), induced squamous cell metaplasia in the murine uterus. Therefore, we have demonstrated that correct regulation of beta-catenin is important for uterine function as well as in the regulation of endometrial epithelial differentiation.
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