Transcription factor PROX1 induces colon cancer progression by promoting the transition from benign to highly dysplastic phenotype.

Détails

ID Serval
serval:BIB_D8971B77174E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Transcription factor PROX1 induces colon cancer progression by promoting the transition from benign to highly dysplastic phenotype.
Périodique
Cancer Cell
Auteur(s)
Petrova T.V., Nykänen A., Norrmén C., Ivanov K.I., Andersson L.C., Haglund C., Puolakkainen P., Wempe F., von Melchner H., Gradwohl G., Vanharanta S., Aaltonen L.A., Saharinen J., Gentile M., Clarke A., Taipale J., Oliver G., Alitalo K.
ISSN
1535-6108
Statut éditorial
Publié
Date de publication
2008
Peer-reviewed
Oui
Volume
13
Numéro
5
Pages
407-419
Langue
anglais
Résumé
The Drosophila transcription factor Prospero functions as a tumor suppressor, and it has been suggested that the human counterpart of Prospero, PROX1, acts similarly in human cancers. However, we show here that PROX1 promotes dysplasia in colonic adenomas and colorectal cancer progression. PROX1 expression marks the transition from benign colon adenoma to carcinoma in situ, and its loss inhibits growth of human colorectal tumor xenografts and intestinal adenomas in Apc(min/+) mice, while its transgenic overexpression promotes colorectal tumorigenesis. Furthermore, in intestinal tumors PROX1 is a direct and dose-dependent target of the beta-catenin/TCF signaling pathway, responsible for the neoplastic transformation. Our data underscore the complexity of cancer pathogenesis and implicate PROX1 in malignant tumor progression through the regulation of cell polarity and adhesion.
Mots-clé
Adenoma, Carcinoma in Situ, Cell Line, Tumor, Colonic Neoplasms, Colorectal Neoplasms, Disease Progression, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Homeodomain Proteins, Humans, Phenotype, Tumor Suppressor Proteins, beta Catenin
Pubmed
Web of science
Open Access
Oui
Création de la notice
01/04/2009 14:49
Dernière modification de la notice
20/08/2019 15:58
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