Reversion of autocrine transformation by a dominant negative platelet-derived growth factor mutant

Mol Cell Biol. 1993 Jul;13(7):4066-76. doi: 10.1128/mcb.13.7.4066-4076.1993.

Abstract

A non-receptor-binding mutant of the platelet-derived growth factor (PDGF) A chain, PDGF-0, was generated by exchanging 7 amino acids in the sequence. The mutant chains formed dimers that were similar to wild-type PDGF-AA with regard to stability and rate of processing to the mature 30-kDa secreted forms. Moreover, the mutant chains formed disulfide-bonded heterodimers with the PDGF B chain in NIH 3T3 cells heterodimer underwent the same processing and secretion as PDGF-AB. Transfection of c-sis-expressing 3T3 cells with PDGF-0 significantly inhibited the transformed phenotype of these cells, as determined by the following criteria. (i) Compared with PDGF-0-negative clones, PDGF-0-producing clones showed a reverted morphology. (ii) Clones producing PDGF-0 grew more slowly than PDGF-0-negative clones, with a fivefold difference in cell number after 14 days in culture. (iii) The expression of PDGF-0 completely inhibited the ability of the c-sis-expressing 3T3 cells to form colonies in soft agar; this inhibition was overcome by the addition of recombinant PDGF-BB to the culture medium, showing that the lack of colony formation of these cells was not due to a general unresponsiveness to PDGF. The specific expression of a PDGF-0/PDGF wild-type heterodimer in COS cells revealed that the affinity of the mutant heterodimer for the PDGF alpha receptor was decreased by approximately 50-fold compared with that of PDGF-AA. Thus, we show that a non-receptor-binding PDGF A-chain mutant neutralizes in a trans-dominant manner the autocrine transforming potential of the c-sis/PDGF B chain by forming low-affinity heterodimers with wild-type PDGF chains. This method of specifically antagonizing the effect of PDGF may be useful in investigations of the role of PDGF in normal and pathological conditions.

MeSH terms

  • 3T3 Cells
  • Animals
  • Cell Line
  • Cell Transformation, Neoplastic / genetics*
  • Cells, Cultured
  • Chromatography, High Pressure Liquid
  • Cloning, Molecular
  • Humans
  • Kinetics
  • Mice
  • Mutation
  • Phenotype
  • Platelet-Derived Growth Factor / genetics*
  • Platelet-Derived Growth Factor / metabolism
  • Precipitin Tests
  • Receptors, Platelet-Derived Growth Factor / metabolism
  • Transfection
  • Tumor Cells, Cultured
  • Up-Regulation

Substances

  • Platelet-Derived Growth Factor
  • Receptors, Platelet-Derived Growth Factor