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

Oncogene. 2003 Sep 18;22(40):6277-88. doi: 10.1038/sj.onc.1206631.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Carbohydrate Metabolism
  • Cell Division / drug effects
  • Dimerization
  • G(M1) Ganglioside / chemistry
  • G(M1) Ganglioside / metabolism
  • Galectin 3 / pharmacology
  • Galectins / genetics
  • Galectins / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Ligands
  • Mass Spectrometry
  • Neuroblastoma / genetics
  • Neuroblastoma / metabolism*
  • Neuroblastoma / pathology*
  • Tumor Cells, Cultured


  • Galectin 3
  • Galectins
  • LGALS7 protein, human
  • Ligands
  • G(M1) Ganglioside