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Titolo:
PROTEIN ZERO, A NERVOUS-SYSTEM ADHESION MOLECULE, TRIGGERS EPITHELIALREVERSION IN HOST CARCINOMA-CELLS
Autore:
DOYLE JP; STEMPAK JG; COWIN P; COLMAN DR; DURSO D;
Indirizzi:
UNIV DUSSELDORF,NEUROL KLIN,NEUROCHEM LAB,MOORENSTR 5 D-40225 DUSSELDORF GERMANY UNIV DUSSELDORF,NEUROL KLIN,NEUROCHEM LAB D-40225 DUSSELDORF GERMANY CUNY MT SINAI SCH MED,BROOKDALE CTR MOLEC BIOL NEW YORK NY 10029 COLUMBIA UNIV COLL PHYS & SURG,CTR NEUROBIOL & BEHAV NEW YORK NY 10032 SUNY HLTH SCI CTR,DEPT ANAT & CELL BIOL BROOKLYN NY 11203 NYU,SCH MED,DEPT CELL BIOL NEW YORK NY 10016 NYU,SCH MED,DEPT DERMATOL NEW YORK NY 10016
Titolo Testata:
The Journal of cell biology
fascicolo: 2, volume: 131, anno: 1995,
pagine: 465 - 482
SICI:
0021-9525(1995)131:2<465:PZANAM>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERCELLULAR ADHERENS JUNCTIONS; INTERMEDIATE FILAMENT NETWORKS; E-CADHERIN; PERIPHERAL MYELIN; A-CAM; DESMOSOMAL PLAQUE; 135-KD RECEPTOR; CULTURED-CELLS; ALPHA-CATENIN; N-CADHERIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
95
Recensione:
Indirizzi per estratti:
Citazione:
J.P. Doyle et al., "PROTEIN ZERO, A NERVOUS-SYSTEM ADHESION MOLECULE, TRIGGERS EPITHELIALREVERSION IN HOST CARCINOMA-CELLS", The Journal of cell biology, 131(2), 1995, pp. 465-482

Abstract

Protein zero (P-o) is the immunoglobulin gene superfamily glycoprotein that mediates the self-adhesion of the Schwann cell plasma membrane that yields compact myelin. HeLa is a poorly differentiated carcinoma cell line that has lost characteristic morphological features of the cervical epithelium from which it originated, Normally, HeLa cells are not self-adherent, However, when P-o is artificially expressed in thisline, cells rapidly aggregate, and P-o concentrates specifically at cell-cell contact sites. Rows of desmosomes are generated at these interfaces, the plasma membrane localization of cingulin and ZO-1, proteins that have been shown to be associated with tight junctions, is substantially increased, and cytokeratins coalesce into a cohesive intracellular network. Immunofluorescence patterns for the adherens junction proteins N-cadherin, alpha-catenin, and vinculin, and the desmosomal polypeptides desmoplakin, desmocollin, and desmoglein, are also markedlyenhanced at the cell surface. Our data demonstrate that obligatory cell-cell adhesion, which in this case is initially brought about by thehemophilic association of P-o molecules across the intercellular cleft, triggers pronounced augmentation of the normally sluggish or sub-basal cell adhesion program in HeLa cells, culminating in suppression ofthe transformed state and reversion of the monolayer to an epithelioid phenotype, Furthermore, this response is apparently accompanied by an increase in mRNA and protein levels for desmoplakin and N-cadherin which are normally associated with epithelial junctions, Our conclusions are supported by analyses of ten proteins we examined immunochemically (P-o, cingulin, ZO-1, desmoplakin, desmoglein, desmocollin, N-cadherin, alpha-catenin, vinculin, and cytokeratin-18), and by quantitativepolymerase chain reactions to measure relative amounts of desmoplakinand N-cadherin mRNAs. P-o has no known signaling properties; the dramatic phenotypic changes we observed are highly likely to have developed in direct response to P-o-induced cell adhesion. More generally, theability of this ''foreign'' membrane adhesion protein to stimulate desmosome and adherens junction formation by augmenting well-studied cadherin-based adhesion mechanisms raises the possibility that perhaps any bona fide cell adhesion molecule, when functionally expressed, can engage common intracellular pathways and trigger reversion of a carcinoma to an epithelial-like phenotype.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 13:24:34