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Oncogene. 2003 Sep 18;22(40):6277-88.

Homodimeric galectin-7 (p53-induced gene 1) is a negative growth regulator for human neuroblastoma cells.

Author information

1
Institut für Molekulare Pathologie, Klinikum der Ruprecht-Karls-Universtiät, Im Neuenheimer Feld 220, 69120 Heidelberg, Germany. juergen_kopitz@med.uni-heidelberg.de

Abstract

The extracellular functions of galectin-7 (p53-induced gene 1) are largely unknown. On the surface of neuroblastoma cells (SK-N-MC), the increased GM1 density, a result of upregulated ganglioside sialidase activity, is a key factor for the switch from proliferation to differentiation. We show by solid-phase and cell assays that the sugar chain of this ganglioside is a ligand for galectin-7. In serum-supplemented proliferation assays, galectin-7 reduced neuroblastoma cell growth without the appearance of features characteristic for classical apoptosis. The presence of galectin-3 blocked this effect, which mechanistically resembles that of galectin-1. By virtue of carbohydrate binding, galectin-7 thus exerts neuroblastoma growth control similar to galectin-1 despite their structural differences. In addition to p53-linked proapoptotic activity intracellularly, galectin-7, acting as a lectin on the cell surface, appears to be capable of reducing cancer cell proliferation in susceptible systems.

PMID:
13679866
DOI:
10.1038/sj.onc.1206631
[Indexed for MEDLINE]

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