Activation of the galectin-1 (L-14-I) gene from nonexpressing differentiated cells by fusion with undifferentiated and tumorigenic cells

Cell Growth Differ. 1994 Jul;5(7):769-75.


Expression of the galectin-1 (L-14-I) gene, elevated in most differentiated and transformed cell lines, has been studied in cell hybrid systems. Fusion of L-14-I nonproducing rat liver differentiated FAO cells with dedifferentiated rat liver BRL3A cells leads to extinction of liver-specific gene expression while L-14-I mRNA levels remain high. Interspecific hybrids produced by fusion of tumorigenic human osteosarcoma 143TK- with FAO cells show loss of both differentiated functions and tumorigenic phenotype and activation of the FAO L-14-I alleles. Increased expression of rat L-14-I alleles was also observed in human osteosarcoma x rat thyroid cells transient heterokaryons. The data presented here show that expression of the L-14-I gene is subject to dominant positive control and that it correlates with loss of differentiation-specific functions, but it is independent from tumorigenicity. L-14-I activation in FAO cells is achieved by treatment with 5-azacytidine. This result suggests that DNA demethylation is responsible or a prerequisite for L-14-I activation in hybrids.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Animals
  • Azacitidine / pharmacology
  • Base Sequence
  • Cell Differentiation / genetics*
  • Cell Fusion*
  • Cells, Cultured
  • Galectin 1
  • Gene Expression Regulation, Neoplastic* / drug effects
  • Genes, Dominant
  • Hemagglutinins / biosynthesis
  • Hemagglutinins / genetics*
  • Humans
  • Liver / cytology
  • Liver Neoplasms, Experimental / pathology
  • Methylation / drug effects
  • Molecular Sequence Data
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / genetics*
  • Neoplastic Stem Cells / metabolism*
  • Osteosarcoma / pathology
  • Rats
  • Tumor Cells, Cultured


  • Galectin 1
  • Hemagglutinins
  • Neoplasm Proteins
  • Azacitidine