Cited by 196Wnt/β-catenin signaling in development and cancerEndometrial and Cervical Cancer TreatmentsCervical Cancer and HPV Research

β-catenin mediates glandular formation and dysregulation of β-catenin induces hyperplasia formation in the murine uterus

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Jeong, J-W, Lee, H S, Franco, H L, Broaddus, R R, Taketo, M M, Tsai, S Y, Lydon, J P, DeMayo, F J·2009·Oncogene

Abstract

Endometrioid adenocarcinoma is the most frequent form of endometrial cancer, usually developing in pre- and peri-menopausal 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 PR(Cre) 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 beta-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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Authors
Jeong, J.-W., Lee, H. S., Franco, H. L., Broaddus, R. R., Taketo, M. M., Tsai, S. Y., Lydon, J. P., & DeMayo, F. J.
Affiliations
  • Baylor College of Medicine (US)
  • MizMedi Hospital (KR)
  • The University of Texas MD Anderson Cancer Center (US)
  • Kyoto University (JP)
Corresponding author
DeMayo, F J
Venue
Oncogene
Published
2008-09-22
Volume
28
Issue
1
Pages
31-40
ISSN
  • 0950-9232 (ISSN-L)
  • 1476-5594
OpenAlex
W1983606581
Cited by
196
References
66
Citations by year
2026: 7 · 2025: 11 · 2024: 8 · 2023: 12 · 2022: 10 · 2021: 5 · 2020: 16 · 2019: 16 · 2018: 12 · 2017: 10 · 2016: 11 · 2015: 6 · 2014: 14 · 2013: 18 · 2012: 10
FWCI
4.12
Type
journal article
Language
en
Open access
Locations
  • Oncogene (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Eye Institute
  • National Cancer Institute (P50CA098258, R01CA77530, R01CA077530, P50CA083639)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (U54 HD-0077495, U54HD007495, R01HD042311, U54HD028934, R03HD077495, R01HD057873, U54-HD-28934)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
  • Health Sciences › Medicine › Obstetrics and Gynecology › Endometrial and Cervical Cancer Treatments
  • Health Sciences › Medicine › Epidemiology › Cervical Cancer and HPV Research
Keywords
β-catenin, CTNNB1, endometrioid carcinoma, endometrial cancer, uterine development, squamous metaplasia, decidual reaction, mouse model, fertility defects
MeSH terms
Animals, Cell Differentiation, Cell Transformation, Neoplastic, Disease Models, Animal, Endometrial Hyperplasia, Endometrium, Female, Infertility, Female, Mice, Mutant Strains, Cell Proliferation, beta Catenin, Mice

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