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J. Biol. Chem., Vol. 263, Issue 36, 19519-19524, 12, 1988
KL Thompson, R Assoian and MR Rosner
Transforming growth factor-beta (TGF-beta) is a potent modulator of cell
growth in many systems. In normal rat kidney (NRK) fibroblasts, TGF-beta
synergizes with epidermal growth factor (EGF) to stimulate growth in soft
agar, a characteristic of the transformed phenotype. Many biochemical
effects of TGF-beta occur at the cell surface. Increased binding of EGF and
synthesis of extracellular matrix components such as fibronectin and
collagen are primary responses of NRK cells to TGF-beta. Although specific
membrane receptors for TGF- beta have been identified, the mechanism of
action of this factor is not well understood. Here we demonstrate that
TGF-beta enhances the expression of the EGF receptor in NRK cells through
an increase in the level of EGF receptor gene transcripts. Analysis of
nuclear run-off transcription levels and mRNA half-lives indicate that the
elevation in EGF-receptor mRNA results from an increase in the rate of
transcription. Dose-response and kinetic studies suggest that the EGF
receptor response to TGF-beta is biphasic, possibly resulting from the
action of multiple TGF-beta receptors. TGF-beta also elevates the levels of
fibronectin and tubulin transcripts in NRK cells; however, the mechanism
differs for each gene. The increase in fibronectin mRNA in response to
TGF-beta results from an increased rate of gene transcription. Tubulin mRNA
levels, in contrast, appear to be post- transcriptionally regulated. These
results implicate TGF-beta as a transcriptional activator of the genes for
both the EGF receptor and fibronectin and suggest the two genes may be
regulated through a common pathway in this cell type.
Transforming growth factor-beta increases transcription of the genes encoding the epidermal growth factor receptor and fibronectin in normal rat kidney fibroblasts
Department of Applied Biological Sciences, Massachusetts Institute of Technology, Cambridge 02139.
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