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(Received for publication, March 4, 1996, and in revised form, August 6, 1996)
From the Vascular endothelial growth factor (VEGF) is an
angiogenic hormone that is produced by and supports the growth of many
types of malignancies. The present study shows that insulin-like growth factor 1 (IGF-I), a mitogen that promotes the propagation of cancers through autocrine and paracrine mechanisms, increases the expression of
mRNA for VEGF and production of VEGF protein by COLO 205 colon carcinoma cells. IGF-I also induces expression of VEGF mRNA in SW620, LSLiM6, and HCT15 colon carcinoma cells showing that this is a
common response to IGF-I. Whereas IGF-I induced VEGF mRNA in each
cell line examined (2.3-12-fold), it induced proliferation only in
COLO 205 and LSLiM6 cells. Thus, the proliferative response induced by
IGF-I and its ability to induce VEGF occur through distinguishable
mechanisms. IGF-I increases the cellular content of VEGF mRNA by
increasing the rate of transcription (5-fold after 4 h) and also
by increasing the half-life of VEGF mRNA (0.6 ± 0.07 h
in control cells to 2.0 ± 0.37 h in IGF-I-treated cells). Monoclonal antibody (
Volume 271, Number 46,
Issue of November 15, 1996
pp. 29483-29488
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
,
,
,
Department of Surgery, University of
California School of Medicine, San Francisco, California 94143,
the ¶ Department of Cardiovascular Research, Genentech, Inc.,
South San Francisco, California 94080, and the 
Department
of Physiology and Biophysics, Indiana University School of Medicine,
Indianapolis, Indiana 46202
IR3) directed against the type 1 IGF receptor significantly attenuated the ability of IGF-I to promote expression of
VEGF mRNA. Interestingly, by itself IR3 acted as a weak agonist and induced a modest increase in the cellular content of VEGF mRNA.
IR3 also promoted tyrosine phosphorylation of the 
subunit of the
IGF-I receptor, and the magnitude of this response was comparable with
that induced by IGF-I. These observations point to a nonlinear
relationship between activation of the IGF-I receptor and induction of
VEGF mRNA. Thus, in addition to its direct, growth stimulatory
effect on transformed cells, IGF-I induces the expression of VEGF which
can promote the progression of cancer by regulating the development of
new blood vessels.
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