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Titolo:
Transforming growth factor-beta 1 mediates epithelial to mesenchymal transdifferentiation through a RhoA-dependent mechanism
Autore:
Bhowmick, NA; Ghiassi, M; Bakin, A; Aakre, M; Lundquist, CA; Engel, ME; Arteaga, CL; Moses, HL;
Indirizzi:
Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Dept Canc Biol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Canc Biol, Nashville, TN 37232 USA Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Dept Med, Nashville,TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 , Dept Med, Nashville,TN 37232 USA
Titolo Testata:
MOLECULAR BIOLOGY OF THE CELL
fascicolo: 1, volume: 12, anno: 2001,
pagine: 27 - 36
SICI:
1059-1524(200101)12:1<27:TGF1ME>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
TGF-BETA RECEPTOR; MICROSATELLITE INSTABILITY; TARGETED DISRUPTION; FOCAL ADHESIONS; CELL-ADHESION; CANCER CELLS; RAC; ACTIVATION; GTPASES; TGF-BETA-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Moses, HL Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Dept Canc Biol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Nashville, TN 37232 USA
Citazione:
N.A. Bhowmick et al., "Transforming growth factor-beta 1 mediates epithelial to mesenchymal transdifferentiation through a RhoA-dependent mechanism", MOL BIOL CE, 12(1), 2001, pp. 27-36

Abstract

Transforming growth factor-beta1 (TGF-beta) can be tumor suppressive, but it can also enhance tumor progression by stimulating the complex process ofepithelial-to-mesenchymal transdifferentiaion (EMT). The signaling pathway(s) that regulate EMT in response to TGF-beta are not well understood. We demonstrate the acquisition of a fibroblastoid morphology, increased N-cadherin expression, loss of junctional E-cadherin localization, and increased cellular motility as markers for TGF-beta -induced EMT. The expression of a dominant-negative Smad3 or the expression of Smad7 to levels that block growth inhibition and transcriptional responses to TGF-beta do not inhibit mesenchymal differentiation of mammary epithelial cells. In contrast, we show that TGF-beta rapidly activates RhoA in epithelial cells, and that blockingRhoA or its downstream target p160(ROCK), by the expression of dominant-negative mutants, inhibited TGF-beta -mediated EMT. The data suggest that TGF-beta rapidly activates RhoA-dependent signaling pathways to induce stress fiber formation and mesenchymal characteristics.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 07:02:49