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Abstract
Interest in the role of the insulin-like growth factor (IGF) axis in growth control
and carcinogenesis has recently been increased by the finding of elevated serum insulin-like
growth factor I (IGF-I) levels in association with three of the most prevalent cancers
in the United States: prostate cancer, colorectal cancer, and lung cancer. IGFs serve
as endocrine, autocrine, and paracrine stimulators of mitogenesis, survival, and cellular
transformation. These actions are mediated through the type 1 IGF-receptor (IGF-1R),
a tyrosine kinase that resembles the insulin receptor. The availability of free IGF
for interaction with the IGF-1R is modulated by the insulin-like growth factor-binding
proteins (IGFBPs). IGFBPs, especially IGFBP-3, also have IGF-independent effects on
cell growth. IGF-independent growth inhibition by IGFBP-3 is believed to occur through
IGFBP-3-specific cell surface association proteins or receptors and involves nuclear
translocation. IGFBP-3-mediated apoptosis is controlled by numerous cell cycle regulators
in both normal and disease processes. IGFBP activity is also regulated by IGFBP proteases,
which affect the relative affinities of IGFBPs, IGFs and IGF-1R. Perturbations in
each level of the IGF axis have been implicated in cancer formation and progression
in various cell types.
Copyright 2000 Wiley-Liss, Inc.