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Titolo:
EFFECT OF CYTOKINES ON TUMOR CELL-ENDOTHELIAL INTERACTIONS
Autore:
COHEN MC; BERETA M; BERETA J;
Indirizzi:
UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT PATHOL & LAB MED,185 S ORANGE AVE NEWARK NJ 07103 JAGIELLONIAN UNIV,INST MOL BIOL PL-31121 KRAKOW POLAND
Titolo Testata:
Indian Journal of Biochemistry & Biophysics
fascicolo: 1-2, volume: 34, anno: 1997,
pagine: 199 - 204
SICI:
0301-1208(1997)34:1-2<199:EOCOTC>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; PROTEIN-KINASE-C; LEUKOCYTE ADHESION MOLECULE-1; FUNCTION-ASSOCIATED ANTIGEN-1; MICROVASCULAR ENDOTHELIUM; SURFACE GLYCOPROTEINS; LYMPHOCYTE ADHERENCE; VCAM-1 EXPRESSION; POTENT INHIBITOR; CARCINOMA CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
M.C. Cohen et al., "EFFECT OF CYTOKINES ON TUMOR CELL-ENDOTHELIAL INTERACTIONS", Indian Journal of Biochemistry & Biophysics, 34(1-2), 1997, pp. 199-204

Abstract

The adherence of tumour cells to microvascular endothelium is believed to be a necessary step in their migration to sites of metastasis. Ithas been proposed that this process occurs when cell surface molecules on tumour cells bind to complementary sites on endothelial cells. The expression of these endothelial-derived cell adhesion molecules appears to be modulated by cytokines, a broad class of protein mediators which play important roles in immune and inflammatory reactions. It hasbeen found by ourselves and others that exposure of endothelium to some cytokines augments the adhesion of inflammatory cells as well as tumour cells in in vitro assays. We used a murine model consisting of P815 mastocytoma cells and microvascular endothelium and found that pretreatment of endothelial monolayers with TNF-alpha, IL-1, LPS or PMA augmented the number of tumour cells that attach in a dose-dependent fashion. FAGS analysis showed that the change in binding was due to an increase in the expression of VCAM-1 on the surface of the endothelial cell. Methylxanthines (caffeine and theophylline) as well. as ''classical'' calcium-mobilizing agents (ionomycin and thapsigargin) inhibited the expression of VCAM-1 in MME. We also studied the possible mechanisms of TNF-alpha signal transduction in endothelial cells. We examined the involvement of protein kinases in the TNF-alpha effect. Although we found that inhibitors of PKC could inhibit the TNF-alpha effect, ourstudies suggest that the ''classical'' PKC pathway is not completely responsible for signaling since TNF-alpha did not cause translocation of PKC to the cell membrane and its effect could not be completely mimicked by PMA. We also studied the effect of TGF-beta on the binding oftumour cells to endothelium. Exposure of endothelium to TGF-beta led to the inhibition of both basal and TNF-alpha enhanced binding of P815cells. Inhibitors of G-proteins do not abolish TGF-beta action, and PKC and PKA activators elicit an opposite effect. However, TGF-beta-mediated inhibition of both basal binding and TNF-alpha-enhanced P815 binding to endothelium is completely abolished in the presence of the protein phosphatase inhibitor okadaic acid suggesting that TGF-beta elicits its effect by stimulating protein phosphatase activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 20:01:10