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Titolo:
Downregulation of E-cadherin and Desmoglein 1 by autocrine hepatocyte growth factor during melanoma development
Autore:
Li, G; Schaider, H; Satyamoorthy, K; Hanakawa, Y; Hashimoto, K; Herlyn, M;
Indirizzi:
Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA Wistar Inst Anat & Biol Philadelphia PA USA 19104 ladelphia, PA 19104 USA Univ Penn, Sch Med, Program Cell & Mol Biol Biomed Grad Studies, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 d Studies, Philadelphia, PA 19104 USA Ehime Univ, Sch Med, Dept Dermatol, Matsuyama, Ehime 790, Japan Ehime Univ Matsuyama Ehime Japan 790 ermatol, Matsuyama, Ehime 790, Japan
Titolo Testata:
ONCOGENE
fascicolo: 56, volume: 20, anno: 2001,
pagine: 8125 - 8135
SICI:
0950-9232(200112)20:56<8125:DOEAD1>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
FACTOR SCATTER FACTOR; PEMPHIGUS-VULGARIS ANTIGEN; CELL-CELL ADHESION; EFFICIENT GENE ACTIVATION; C-MET; INTERMEDIATE FILAMENTS; MALIGNANT-MELANOMA; CATENIN COMPLEX; FACTOR-RECEPTOR; BETA-CATENIN;
Keywords:
HGF; autocrine; E-cadherin; Desmoglein; melanoma;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
102
Recensione:
Indirizzi per estratti:
Indirizzo: Herlyn, M Wistar Inst Anat & Biol, 3601 Spruce St, Philadelphia, PA 19104 USA Wistar Inst Anat & Biol 3601 Spruce St Philadelphia PA USA 19104
Citazione:
G. Li et al., "Downregulation of E-cadherin and Desmoglein 1 by autocrine hepatocyte growth factor during melanoma development", ONCOGENE, 20(56), 2001, pp. 8125-8135

Abstract

During melanoma development, transformed cells evade keratinocyte-mediatedcontrol by downregulating cell adhesion molecules. This study investigatedthe regulation of cell adhesion by hepatocyte growth factor (HGF) in melanoma. Melanocytes and two melanoma lines, WM164 and WM35, expressed normal level E-cadherin and Desmoglein 1, whereas most melanomas (18 out of 20) expressed no E-cadherin and significantly reduced Desmoglein 1. Overexpressionof dominant negative E-cadherin and Desmoglein in melanocytes demonstratedthat both molecules contribute to adhesion between melanocytes and keratinocytes. In contrast to melanocytes, most melanomas expressed HGF. All melanocytic cells expressed the HGF receptor c-Met, and autocrine HGF caused constitutive activation of c-Met, MAPK and PI3K. When autocrine activation wasinduced with HGF-expressing adenovirus, E-cadherin and Desmoglein I were decreased in melanocytes, WM164 and WM35. MAPK inhibitor PD98059 and PI3K inhibitor wortmannin partially blocked the downregulation, suggesting that both pathways are involved in this process. c-Met was coimmunoprecipitated with E-cadherin, Desmoglein I and Plakoglobin, suggesting that they form a complex (es) that acts to regulate intercellular adhesion. Together, the results indicate that autocrine HGF decouples melanomas from keratinocytes by downregulating E-cadherin and Desmoglein 1, therefore frees melanoma cells from the control by keratinocytes and allows dissemination of the tumor mass.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 22:38:47