P. Zalecki et al., MODULATION BY INTERLEUKIN-2 OF CELLULAR-RESPONSE TO FIBROBLAST GROWTH-FACTOR-I IN F69-3 FIBROSARCOMA CELLS, Experimental cell research, 244(1), 1998, pp. 61-70
FGF-1 stimulated DNA synthesis and induced expression of IL-2 receptor
s in the murine fibrosarcoma cell line, F69-3. Concomitant treatment w
ith IL-2 abolished the stimulation of DNA synthesis, but not binding o
f FGF-1 to the FGF-receptors or subsequent endocytosis of the bound gr
owth factor. Also, it did not inhibit activation of the FGF-receptor t
yrosine kinase or stimulation of the downstream effector, MAP kinase.
Treatment with IL-2 prevented transport of FGF-1 to the nuclear fracti
on in a time- and dose-dependent manner that parallelled the inhibitio
n of FGF-1 stimulated DNA synthesis, The data support our earlier find
ing that transport of FGF-1 to the nucleus is an important event in th
e mechanism of stimulation of DNA synthesis induced by the growth fact
or, and they demonstrate that treatment with a cytokine can modulate t
he cellular response to FGF-1. (C) 1998 Academic Press.