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

Jürgen Kopitz, Sabine André, Carolina Von Reitzenstein, Kees Versluis, Herbert Kaltner, Roland J. Pieters, Kojiro Wasano, Ichiro Kuwabara, Fu-Tong Liu, Michael Cantz, Albert J R Heck, Hans Joachim Gabius

Research output: Contribution to journalArticlepeer-review

135 Scopus citations


The extracellular functions of galectin-7 (p53-induced gene 1) are largely unknown. On the surface of neuroblastoma cells (SK-N-MC), the increased GM 1 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.

Original languageEnglish (US)
Pages (from-to)6277-6288
Number of pages12
Issue number40
StatePublished - Sep 18 2003


  • Apoptosis
  • Cell growth
  • Galectin
  • Ganglioside
  • Mass spectrometry
  • Neuroblastoma

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics


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