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Titolo:
E-cadherin regulates cell growth by modulating proliferation-dependent beta-catenin transcriptional activity
Autore:
Stockinger, A; Eger, A; Wolf, J; Beug, H; Foisner, R;
Indirizzi:
Univ Vienna, Bioctr, Dept Biochem & Mol Cell Biol, A-1030 Vienna, Austria Univ Vienna Vienna Austria A-1030 Mol Cell Biol, A-1030 Vienna, Austria Res Inst Mol Pathol, A-1030 Vienna, Austria Res Inst Mol Pathol Vienna Austria A-1030 Pathol, A-1030 Vienna, Austria
Titolo Testata:
JOURNAL OF CELL BIOLOGY
fascicolo: 6, volume: 154, anno: 2001,
pagine: 1185 - 1196
SICI:
0021-9525(20010917)154:6<1185:ERCGBM>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
COLON-CARCINOMA CELLS; MEMBRANE-PROXIMAL REGION; CYTOPLASMIC DOMAIN; TUMOR-SUPPRESSOR; XENOPUS EMBRYOS; AXIS FORMATION; NEOPLASTIC TRANSFORMATION; FUNCTIONAL INTERACTION; NUCLEAR TRANSLOCATION; RECEPTOR ACTIVATION;
Keywords:
carcinogenesis; catenins; cell proliferation; E-cadherin; LEF-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
73
Recensione:
Indirizzi per estratti:
Indirizzo: Foisner, R Univ Vienna, Bioctr, Dept Biochem & Mol Cell Biol, Dr Bohrgasse9, A-1030 Vienna, Austria Univ Vienna Dr Bohrgasse 9 Vienna Austria A-1030 enna, Austria
Citazione:
A. Stockinger et al., "E-cadherin regulates cell growth by modulating proliferation-dependent beta-catenin transcriptional activity", J CELL BIOL, 154(6), 2001, pp. 1185-1196

Abstract

beta -Catenin is essential for E-cadherin-mediated cell adhesion in epithelial cells, but it also forms nuclear complexes with high mobility group transcription factors. Using a mouse mammary epithelial cell system, we have shown previously that conversion of epithelial cells to a fibroblastoid phenotype (epithelial-mesenchymal transition) involves downregulation of E-cadherin and upregulation of beta -catenin transcriptional activity. Here, we demonstrate that transient expression of exogenous E-cadherin in both epithelial and fibroblastoid cells arrested cell growth or caused apoptosis, depending on the cellular E-cadherin levels. By expressing E-cadherin subdomains, we show that the growth-suppressive effect of E-cadherin required the presence of its cytoplasmic beta -catenin interaction domain and/or correlated strictly with the ability to negatively interfere with beta -catenin transcriptional activity. Furthermore, coexpression of beta -catenin or lymphoid enhancer binding factor-1 or T cell factor 3 with E-cadherin rescued beta -catenin transcriptional activity and counteracted E-cadherin-mediated cell cycle arrest. Stable expression of E-cadherin in fibroblastoid cells decreased beta -catenin activity and reduced cell growth. Since proliferating cells had a higher beta -catenin activity than G1 phase-arrested or contact-inhibited cells, we conclude that beta -catenin transcriptional activity is essential for cell proliferation and can be controlled by E-cadherin in acell adhesion-independent manner.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 15:32:15