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Titolo:
The alpha v beta 6 integrin regulates its own expression with cell crowding: Implications for tumour progression
Autore:
Niu, J; Gu, X; Ahmed, N; Andrews, S; Turton, J; Bates, R; Agrez, M;
Indirizzi:
Univ Newcastle, Fac Med & Hlth Sci, Discipline Surg Sci, Callaghan, NSW 2308, Australia Univ Newcastle Callaghan NSW Australia 2308 allaghan, NSW 2308, Australia John Hunter Hosp, Hunter Area Pathol Serv, Newcastle, NSW, Australia John Hunter Hosp Newcastle NSW Australia Serv, Newcastle, NSW, Australia Univ Newcastle, Fac Med & Hlth Sci, Discipline Med Biochem, Newcastle, NSW2308, Australia Univ Newcastle Newcastle NSW Australia 2308 Newcastle, NSW2308, Australia
Titolo Testata:
INTERNATIONAL JOURNAL OF CANCER
fascicolo: 1, volume: 92, anno: 2001,
pagine: 40 - 48
SICI:
0020-7136(20010401)92:1<40:TAVB6I>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; COLON-CARCINOMA CELLS; GELATINASE-B SECRETION; IV COLLAGENASE; HUMAN KERATINOCYTES; TISSUE INHIBITOR; CANCER CELLS; FIBRONECTIN; LINES; MODULATION;
Keywords:
alpha v beta 6; integrins; cell density; colon cancer; gelatinase B;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Agrez, M Univ Newcastle, Fac Med & Hlth Sci, Discipline Surg Sci, Callaghan, NSW 2308, Australia Univ Newcastle Callaghan NSW Australia 2308 NSW 2308, Australia
Citazione:
J. Niu et al., "The alpha v beta 6 integrin regulates its own expression with cell crowding: Implications for tumour progression", INT J CANC, 92(1), 2001, pp. 40-48

Abstract

Expression of the growth-promoting integrin alphav betaB in colon cancer cells induces gelatinase B secretion and activation, the inhibition of whichabolishes alphav beta6-mediated tumour cell growth within a collagen matrix. Herein, we show that high cell density selectively enhances alphav beta6expression in a protein kinase C (PKC)-dependent manner in preference to other beta integrin subunits, resulting in a marked increase in gelatinase Bsecretion as cells reach confluence. Moreover, PKC activity increases withcell confluence, and the rise in PKC activity is much greater for alphav beta6-expressing cells than for colon cancer cells which lack alphav beta6. We propose a self-perpetuating system of colon cancer progression in which the integrin alphav beta6 provides a means of sustaining tumour cell proliferation. In this model, alphav beta6 regulates its own expression via a PKC-mediated signalling pathway as tumour cells become crowded and quiescent. The alphav beta6-mediated induction of gelatinase B secretion facilitates pericellular matrix degradation, which helps overcome crowding and restores cell proliferation, (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/10/20 alle ore 15:43:30