In tumor cells expressing platelet-derived growth factor (PDGF) ligand(s) and receptor(s), immunoblot analysis established tyrosine phosphorylation of PDGF receptors (PDGFRs) in the absence of any exogenous ligand, implying chronic receptor activation. Exposure to suramin resulted in diminished receptor autophosphorylation and/ or up-regulation of receptor protein. In a subset of such tumor lines, there was a marked reduction in DNA synthesis in response to suramin or PDGF-neutralizing antiserum. These findings demonstrate that autocrine PDGF stimulation contributes to proliferation of some human tumors and that agents which interfere with ligand-receptor interactions at the cell surface can significantly interfere in this process.
|Number of pages
|Published - Jul 1992
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cancer Research