Syndecan-1-dependent homotypic cell adhesion in HT58 lymphoma cells

Citation
A. Sebestyen et al., Syndecan-1-dependent homotypic cell adhesion in HT58 lymphoma cells, TUMOR BIOL, 21(6), 2000, pp. 349-357
Citations number
35
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
TUMOR BIOLOGY
ISSN journal
10104283 → ACNP
Volume
21
Issue
6
Year of publication
2000
Pages
349 - 357
Database
ISI
SICI code
1010-4283(200011/12)21:6<349:SHCAIH>2.0.ZU;2-D
Abstract
Objectives: Many cellular functions are controlled by cell-cell and cell-ma trix interactions. It has recently been found that syndecans, transmembrane heparan sulphate (HS) proteoglycans, can act as receptors or coreceptors a nd modulate cell adhesion. Our aim was to study the role of syndecan-1 in t he aggregation of human lymphoma cells, and to investigate its effect on ce ll survival. Methods: Immunocytochemistry, confocal laser scanning microsco py, flow cytometry and aggregation/reaggregation bio-assays were used on HT 58, BL41/95 and Raji lymphoma cell lines. Results: Bio-assays showed that t he aggregation of HT58 cells was inhibited by heparin, HS, removal of the H S chain and binding of the anti-syndecan-1 monoclonal antibody. In the sear ch for a counter-receptor of syndecan-1, several adhesion molecules were te sted, but none of them proved to be the adhesion partner. In the case of he paritinase/trypsin digestion with long-term inhibition of HS synthesis (sod ium chlorate treatment), the inhibited aggregation was accompanied by cell cycle arrest and the induction of apoptosis. Conclusions: The results obtai ned showed that surface syndecan-1 expression contributes to homotypic adhe sion. In addition, HS chains, including those on syndecan-1, take part in t he regulation of cell proliferation and active cell death in HT58 lymphoma cells. Copyright (C) 2000 S. Karger AG. Basel.