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

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.

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Acknowledgements

We gratefully acknowledge Dr JL Wang for kindly providing the expression vector for murine galectin-3, Dr BB Namirha for helpful advice and L Mantel for excellent technical assistance. Furthermore, we are indebted to the EURO-conference program and the DAAD/NSF cooperation program for travel grants, and to the Wilhelm Sander-Stiftung (Munich, Germany) for generous financial support.

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Correspondence to Jürgen Kopitz.

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Dedicated to Professor Dr F Cramer on the occasion of his 80th birthday

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Kopitz, J., André, S., von Reitzenstein, C. et al. Homodimeric galectin-7 (p53-induced gene 1) is a negative growth regulator for human neuroblastoma cells. Oncogene 22, 6277–6288 (2003). https://doi.org/10.1038/sj.onc.1206631

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