Modulation by Interleukin-2 of Cellular Response to Fibroblast Growth Factor-1 in F69-3 Fibrosarcoma Cells

FGF-1 stimulated DNA synthesis and induced expression of IL-2 receptors in the murine fibrosarcoma cell line, F69-3. Concomitant treatment with IL-2 abolished the stimulation of DNA synthesis, but not binding of FGF-1 to the FGF-receptors or subsequent endocytosis of the bound growth factor. Also, i...

Full description

Saved in:

Bibliographic Details
Published in:	Experimental cell research Vol. 244; no. 1; pp. 61 - 70
Main Authors:	Zał ę, Piotr, Radzikowski, Czesław, Olsnes, Sjur, Wi ę, Antoni
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 10-10-1998
Subjects:	Animals Calcium-Calmodulin-Dependent Protein Kinases - metabolism Cell Nucleus - metabolism DNA, Neoplasm - biosynthesis Enzyme Activation - drug effects Fibroblast Growth Factor 1 Fibroblast Growth Factor 2 - antagonists & inhibitors Fibroblast Growth Factor 2 - metabolism Fibroblast Growth Factor 2 - pharmacology Fibrosarcoma - metabolism Humans Interleukin-2 - pharmacology Mice Mice, Inbred BALB C Mice, Nude Protein Binding - drug effects Receptors, Fibroblast Growth Factor - metabolism Signal Transduction - drug effects Tumor Cells, Cultured
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	FGF-1 stimulated DNA synthesis and induced expression of IL-2 receptors in the murine fibrosarcoma cell line, F69-3. Concomitant treatment with IL-2 abolished the stimulation of DNA synthesis, but not binding of FGF-1 to the FGF-receptors or subsequent endocytosis of the bound growth factor. Also, it did not inhibit activation of the FGF-receptor tyrosine kinase or stimulation of the downstream effector, MAP kinase. Treatment with IL-2 prevented transport of FGF-1 to the nuclear fraction in a time- and dose-dependent manner that parallelled the inhibition of FGF-1 stimulated DNA synthesis. The data support our earlier finding that transport of FGF-1 to the nucleus is an important event in the mechanism of stimulation of DNA synthesis induced by the growth factor, and they demonstrate that treatment with a cytokine can modulate the cellular response to FGF-1.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0014-4827 1090-2422
DOI:	10.1006/excr.1998.4187