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Titolo:
TUMOR MALIGNANCY DEFINED BY ABERRANT GLYCOSYLATION AND SPHINGO(GLYCO)LIPID METABOLISM
Autore:
HAKOMORI S;
Indirizzi:
PACIFIC NW RES FDN,BIOMEMBRANE DIV,720 BROADWAY SEATTLE WA 98122 UNIV WASHINGTON,DEPT PATHOBIOL SEATTLE WA 98195 UNIV WASHINGTON,DEPT MICROBIOL SEATTLE WA 98195
Titolo Testata:
Cancer research
fascicolo: 23, volume: 56, anno: 1996,
pagine: 5309 - 5318
SICI:
0008-5472(1996)56:23<5309:TMDBAG>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARBOHYDRATE-CARBOHYDRATE INTERACTION; ALPHA-5-BETA-1 INTEGRIN RECEPTOR; CONTROLLING CELL MOTILITY; LYMPH-NODE INVOLVEMENT; GROWTH-FACTOR RECEPTOR; COLON-CARCINOMA CELLS; HUMAN LUNG CARCINOMAS; E-SELECTIN EXPRESSION; HUMAN-MELANOMA CELLS; ROUS-SARCOMA VIRUS;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
133
Recensione:
Indirizzi per estratti:
Citazione:
S. Hakomori, "TUMOR MALIGNANCY DEFINED BY ABERRANT GLYCOSYLATION AND SPHINGO(GLYCO)LIPID METABOLISM", Cancer research, 56(23), 1996, pp. 5309-5318

Abstract

Aberrant glycosylation expressed in glycosphingolipids and glycoproteins in tumor cells has been implicated as an essential mechanism in defining stage, direction, and fate of tumor progression. This general concept is supported by results from three lines of study: (a) Numerousclinicopathological studies have shown a clear correlation between aberrant glycosylation status of primary tumor and invasive/metastatic potential of human cancer as reflected by 5- or 10-year survival rates of patients.(b) Carbohydrates expressed in tumor cells are either adhesion molecules per se or modulate adhesion receptor function. Some aredirectly involved in cell adhesion. They are recognized by selectins or other carbohydrate-binding proteins or by complementary carbohydrates (through carbohydrate-carbohydrate interaction). N- or O-glycosylation of functionally important membrane components may alter tumor celladhesion or motility in a direction that either promotes or inhibits invasion and metastasis. Examples of such receptors are E-cadherin, integrins, immunoglobulin family receptors (e.g., CD44), and lysosome-associated membrane protein. (c) Gangliosides and sphingolipids modulatetransmembrane signaling essential for tumor cell growth, invasion, and metastasis. The transducer molecules susceptible to gangliosides andsphingolipids include integrin receptors, tyrosine kinase-linked growth factor receptors, protein kinase C, and G-protein-linked receptor affecting protein kinase A. Some glycosphingolipids (e.g., Gb3Cer, Le(y)), ceramide, and sphingosine induce tumor cell differentiation and subsequent apoptosis. Shedded gangliosides may block immunogenicity of tumor cells, providing conditions favorable for ''escape'' from immunological suppression of tumor growth by the host. Various reagents that block carbohydrate-mediated tumor cell adhesion or block glycosylationprocessing have been shown to inhibit tumor cell metastasis. This provides the basis for further development of ''anti-adhesion therapy. '' Ganglioside analogues and sphingolipid analogues that inhibit protein kinase C and receptor-associated tyrosine kinase have been applied forinhibition of metastasis. A crucial mechanism for inhibition of metastasis by these reagents may involve blocking of transmembrane signaling for expression of P- and E-selectin. This provides the basis for development of ''ortho-signaling therapy.''

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Documento generato il 28/11/20 alle ore 08:32:30