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(Received for publication, February 6, 1996, and in revised form, August 26, 1996)
From the Expression of epidermal growth factor receptor
(EGF-R) antisense RNA results in a drastic reduction of EGF-R levels in
the human carcinoma KB cell line and induces a reversion of their transformed phenotype (Moroni, M. C., Willingham, M. C., and Beguinot, L. (1992) J. Biol. Chem. 267, 2714-2722). We used
parental and EGF-R antisense KB clones as a genetic system to study, in
the same cell line, the role of transforming growth factor
Volume 271, Number 47,
Issue of November 22, 1996
pp. 30290-30296
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
in the Human Carcinoma KB Cell Line
,
,
,
¶
and
Laboratory of Molecular Oncology,
(TGF-
) in the establishment and maintenance of the transformed
phenotype. KB cells produce TGF-
mRNA, and their conditioned
medium is able to sustain growth of antisense cells, mimicking the
effect of exogenous EGF or TGF-
. In antisense cells there is a
marked reduction of TGF-
mRNA steady-state levels. In addition,
the decrease in TGF-
parallels the levels of residual EGF-R in the
various antisense clones, indicating a direct correlation between
receptors and growth factor levels. The addition of exogenous TGF-
(10 ng/ml) to antisense clones induces TGF-
levels. The half-life of
TGF-
mRNA is 40-60 min in antisense cells and more than 8 h in parental KB cells, as determined by actinomycin D decay curves.
This result indicates a predominant regulation of TGF-
mRNA at
the post-transcriptional level. Nuclear run-on experiments show that
there is only a marginal effect at the transcriptional level. We
conclude that the autocrine loop responsible for the transformed
phenotype of the human carcinoma KB cell line is dependent on both
elevated levels of EGF-R and the presence of TGF-
. In addition,
TGF-
is able to induce its own mRNA via a signal due to
activation of the EGF-R acting predominantly at the
post-transcriptional level.
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