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Kopitz, J. et al.

Kopitz, André, von Reitzenstein, Versluis, Kaltner, Pieters, Wasano, Kuwabara, Liu, Cantz, Heck, Gabius,

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

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.[1]

References

Homodimeric galectin-7 (p53-induced gene 1) is a negative growth regulator for human neuroblastoma cells. Kopitz, J., André, S., von Reitzenstein, C., Versluis, K., Kaltner, H., Pieters, R.J., Wasano, K., Kuwabara, I., Liu, F.T., Cantz, M., Heck, A.J., Gabius, H.J. Oncogene (2003) [Pubmed]

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