The growth of CG-1 human nasopharyngeal carcinoma cell line and five of its randomly selected, single cell-derived subline cells is inhibited by bFGF in an autocrine and paracrine manner. In contrast, aFGF, which has a 55% homology in amino acid sequence with bFGF, stimulates cell growth. Basic FGF binds to specific cell surface high-affinity receptor sites with an apparent K(d) of 105 pM. Of the two lines examined, the high-affinity binding sites for bFGF are calculated to be 1200 and 2600 per cell. The biological effect of bFGF is conveyed through its binding to the high-affinity receptor sites and the binding is dependent on the presence of cell surface heparin-like molecules, as treatment of cells with heparitinase or sodium chlorate abolishes high-affinity binding and growth inhibition. In contrast, similar treatment has no obvious effect on the growth-stimulatory effect of aFGF. Experimental results are also presented showing that the growth inhibition by bFGF is mediated through type I FGF receptors. These results suggest that bFGF and aFGF act via distinct receptor types to oppositely regulate the growth of CG-1 and subline cells.
