Upregulation of TCF4 expression as a transcriptional target of β-catenin/p300 complexes during trans-differentiation of endometrial carcinoma cells

Nuclear stabilization of β -catenin and its interaction with TCF/LEF factors are key events in transduction of the Wnt/ β -catenin signal pathway. Our previous study indicated that nuclear β -catenin accumulation provides an initial signal for trans -differentiation toward the squamoid phenotype of...

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Bibliographic Details
Published in:Laboratory investigation 2005-06, Vol.85 (6), p.768-779
Main Authors: Saegusa, Makoto, Hashimura, Miki, Kuwata, Takeshi, Hamano, Mieko, Okayasu, Isao
Format: Article
Language:English
Subjects:
Base Sequence
beta Catenin
Biological and medical sciences
Biotechnology
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - pathology
Cell Differentiation
Cell Line, Tumor
Cytoskeletal Proteins - metabolism
DNA Primers
DNA-Binding Proteins - genetics
Endometrial Neoplasms - genetics
Endometrial Neoplasms - pathology
Endometrial Neoplasms - surgery
Female
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Neoplastic
Helix-Loop-Helix Motifs
Humans
Hysterectomy
Investigative techniques, diagnostic techniques (general aspects)
Laboratory Medicine
Medical sciences
Medicine
Medicine & Public Health
Metaplasia
Nuclear Proteins - metabolism
Pathology
Phenotype
Promoter Regions, Genetic
research-article
Reverse Transcriptase Polymerase Chain Reaction
TCF Transcription Factors
Trans-Activators - metabolism
Transcription Factor 7-Like 2 Protein
Transcription Factors - genetics
Transcription, Genetic
Transfection
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Summary:Nuclear stabilization of β -catenin and its interaction with TCF/LEF factors are key events in transduction of the Wnt/ β -catenin signal pathway. Our previous study indicated that nuclear β -catenin accumulation provides an initial signal for trans -differentiation toward the squamoid phenotype of endometrial carcinoma (Em Ca) cells in a TCF4-dependent manner, which makes this a possible factor for a positive prognosis. However, little is known about regulation of TCF4 expression in Em Cas. We show here that β -catenin can directly induce transcription from the TCF4 promoter, the effect being enhanced by the p300 coactivator. In clinical cases, nuclear β -catenin accumulation was found to frequently overlap with TCF4 immunoreactivity in morules and surrounding glandular carcinoma lesions, showing a significant positive correlation ( r =0.82, P
ISSN:0023-6837
1530-0307
DOI:10.1038/labinvest.3700273