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Mechanism of differential inhibition of factor-dependent cell proliferation
by transforming growth factor-beta 1: selective uncoupling of FMS from MYC
AR Chen and LR Rohrschneider
Department of Cell Biology, Fred Hutchinson Cancer Research Center,
Seattle, WA 98104.
Transforming growth factor-beta 1 (TGF-beta 1) selectively modulates
hematopoietic cell proliferation. The proliferation of FDC-P1 clone MAC-
11, a factor-dependent murine myeloid progenitor cell line, was inhibited
differentially by TGF-beta 1: strongly in macrophage colony- stimulating
factor (M-CSF), mildly in interleukin-3, and not at all in
granulocyte-macrophage-CSF (GM-CSF). Flow cytometry and Western blots
showed an unexpected increase in expression of FMS, the receptor for M-
CSF, in response to TGF-beta 1. Metabolic labeling with 35S-methionine
showed that synthesis of FMS protein accelerated in response to TGF- beta
1, whereas its degradation was unaffected. Northern analyses showed a rapid
increase in c-fms RNA after the addition of TGF-beta 1. TGF-beta 1 did not
affect kinase activity, cellular phosphotyrosine response, or
internalization of FMS. However, TGF-beta 1 inhibited the induction by
M-CSF of c-myc RNA analyzed on Northern blots and protein detected by
radioimmuno-precipitation. TGF-beta 1 did not affect induction of c-myc
expression by GM-CSF or induction of c-fos or c-jun by M-CSF. Therefore,
FMS and the GM-CSF receptor induce c-myc via signal transduction pathways
that differ in that only the former is inhibited by TGF-beta 1. This
inhibition may account for the selective growth regulation by TGF-beta 1.
Volume 81,
Issue 10,
pp. 2539-2546,
05/15/1993
Copyright © 1993 by The American Society of Hematology
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