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J Biol Chem, Vol. 273, Issue 16, 9994-10003, April 17, 1998
From the Division of Medical Oncology, Department of Medicine,
University of Texas Health Science Center, San Antonio,
Texas 78284-7884 and the Because insulin-like growth factor-I (IGF-I),
insulin, and interleukin-4 (IL-4) have known biological effects in
breast cancer cells and signal through insulin-receptor substrate (IRS)
adaptor proteins, we examined the expression and function of IRS-1 and IRS-2 in breast tumors and cell lines. IRS-1 and IRS-2 were expressed by cell lines and primary breast tumor specimens. IGF-I, insulin, and
IL-4 treatment of MCF-7 and ZR-75, and IGF-I treatment of T47-D breast
cancer cells, resulted in much greater tyrosine phosphorylation of
IRS-1 compared with IRS-2. Furthermore, IGF-I stimulated greater tyrosine phosphorylation of IRS-1 than either insulin or IL-4. IGF-I
treatment also enhanced association of the p85 regulatory subunit of
phosphatidylinositol 3-kinase with IRS-1 and stimulated increased
enzymatic activity compared with IL-4 and insulin in all three cell
lines. Similarly, mitogen-activated protein kinase activity was greater
in IGF-I-stimulated cells. To determine the functional significance of
the activation of these pathways, we inhibited activation of
phosphatidylinositol 3-kinase with wortmannin and mitogen-activated
protein kinase with PD098059. Both compounds inhibited IGF-stimulated
growth, suggesting that both pathways contributed to the mitogenic
response to IGF-I. We conclude that IRS-1, and not IRS-2, is the
predominant signaling molecule activated by IGF-I, insulin, and IL-4.
Furthermore, enhanced tyrosine phosphorylation of IRS-1 by IGF-I,
compared with either insulin or IL-4, is associated with greater
activation of mitogenic downstream signaling pathways resulting in
enhanced cell growth.
Insulin Receptor Substrate-1 is the Predominant Signaling
Molecule Activated by Insulin-like Growth Factor-I, Insulin, and
Interleukin-4 in Estrogen Receptor-positive Human Breast Cancer
Cells
, and Research Division, Joslin
Diabetes Center, Harvard Medical School, Boston,
Massachusetts 02215
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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