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

JEONG, J-W ; LEE, H. S ; FRANCO, H. L ; BROADDUS, R. R ; TAKETO, M. M ; TSAI, S. Y ; LYDON, J. P ; DEMAYO, F. J

Oncogene, 2009-01, Vol.28 (1), p.31-40 [Periódico revisado por pares]

Basingstoke: Nature Publishing Group

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Título:
β-catenin mediates glandular formation and dysregulation of β-catenin induces hyperplasia formation in the murine uterus
Autor: JEONG, J-W ; LEE, H. S ; FRANCO, H. L ; BROADDUS, R. R ; TAKETO, M. M ; TSAI, S. Y ; LYDON, J. P ; DEMAYO, F. J
Assuntos: Animals ; beta Catenin - genetics ; beta Catenin - physiology ; Biological and medical sciences ; Cell adhesion molecules ; Cell differentiation ; Cell Differentiation - genetics ; Cell physiology ; Cell Proliferation ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - pathology ; Disease Models, Animal ; Endometrial cancer ; Endometrial Hyperplasia - genetics ; Endometrial Hyperplasia - pathology ; Endometrium - growth & development ; Endometrium - pathology ; Female ; Fundamental and applied biological sciences. Psychology ; Genetic aspects ; Health aspects ; Infertility, Female - genetics ; Mice ; Mice, Mutant Strains ; Molecular and cellular biology ; Risk factors
É parte de: Oncogene, 2009-01, Vol.28 (1), p.31-40
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: 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.
Editor: Basingstoke: Nature Publishing Group
Idioma: Inglês

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

JEONG, J-W ; LEE, H. S ; FRANCO, H. L ; BROADDUS, R. R ; TAKETO, M. M ; TSAI, S. Y ; LYDON, J. P ; DEMAYO, F. J

Basingstoke: Nature Publishing Group

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