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Transforming growth factor
Volume 270,
Number 23,
Issue of June 9, pp. 14154-14159, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
Modulates the Expression
of Integrin
in Human Colon Carcinoma
FET Cells
(TGF-) has been
extensively studied as an exogenous agent that stimulates the
expression of extracellular matrix proteins and their cell-surface
integrin receptors in a variety of cell types. However, the recent
demonstration of autocrine TGF- growth effects in a number of cell
types suggests that the steady-state expression of extracellular matrix
and integrin proteins and their biological activity may also be under
autocrine TGF- control. Previously, we reported that repression of
autocrine TGF-
activity by constitutive expression of
a full-length TGF- antisense cDNA led to abrogation of
autocrine negative TGF- and, as a result, increased tumorigenicity
and anchorage-independent growth of a poorly tumorigenic,
well-differentiated colon carcinoma cell line designated FET (Wu, S.,
Theodorescu, D., Kerbel, R. S., Willson, J. K. V., Mulder, K. M.,
Humphrey, L. E., and Brattain, M. G.(1992) J. Cell Biol. 116,
187-196). Consequently, we have used this model system to study
the effects of repression of autocrine TGF- activity
on the expression of integrin 
and
integrin -mediated cell adhesion to
fibronectin. The expression of the integrin subunit
was reduced in TGF- antisense transfected FET cells at
both mRNA and protein levels as determined by RNase protection assays
and immunoprecipitation, respectively. Autocrine TGF- had no effect on the transcription of integrin and subunits, indicating that autocrine
TGF- may regulate integrin
expression at the
post-transcriptional level. The diminished expression of integrin
on the cell surface led to the
reduced adhesion of TGF- antisense transfected cells
to fibronectin. This phenomenon could be reversed by treatment with
exogenous TGF-.
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