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Volume 272, Number 26,
Issue of June 27, 1997
pp. 16514-16520
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
Membrane-associated Insulin-like Growth Factor-binding Protein-3
Inhibits Insulin-like Growth Factor-I-induced Insulin-like Growth
Factor-I Receptor Signaling in Ishikawa Endometrial Cancer Cells
(Received for publication, December 3, 1996, and in revised form, April 18, 1997)
Michael
Karas
,
Michael
Danilenko
,
Daniel
Fishman
,
Derek
LeRoith
§
,
Joseph
Levy
and
Yoav
Sharoni
From the Departments of Clinical Biochemistry and
Immunology and Microbiology, Faculty of Health
Sciences, Ben-Gurion University of the Negev, Soroka Medical Center
of Kupat Holim, Beer-Sheva 84105, Israel and the
§ Diabetes Branch, NIDDK, National Institutes of Health,
Bethesda, Maryland 20892
The function of cell surface-associated
insulin-like growth factor-binding proteins (IGFBPs) is controversial.
Both inhibition and facilitation of IGF action as well as
IGF-independent effects have been reported. We examined the influence
of endogenous cell surface-associated IGFBPs on IGF-I receptor (IGF-IR)
function in Ishikawa endometrial cancer cells by comparing the effects of IGF-I and its truncated analog des-(1-3)-IGF-I on several
components of the IGF-IR signal transduction pathway in the absence of
significant amounts of soluble IGFBPs. IGF-I and des-(1-3)-IGF-I are
known to have similar affinities for IGF-IR, although the affinity of des-(1-3)-IGF-I for IGFBPs is greatly reduced. Here we show that the
two ligands were equipotent not only in IGF-IR binding but also in
receptor activation in NIH 3T3 cells overexpressing IGF-IR and
possessing a relatively small number of cell surface-associated IGFBPs.
In contrast, des-(1-3)-IGF-I manifested a remarkably higher potency as
compared with IGF-I in inducing short and middle term cellular
responses in IGF-IR-transfected Ishikawa endometrial cancer cells
possessing a high number of both the receptor and the cell
membrane-bound IGFBP-3. Thus, this difference in the effects of IGF-I
and des-(1-3)-IGF-I can be attributed to the attenuation of
IGF-I-mediated IGF-IR signaling by membrane-bound IGFBP-3.

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Copyright © 1997 by the American Society for Biochemistry and Molecular Biology.
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