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Induction of transforming growth factor-beta 1 (TGF-beta 1), receptor
expression and TGF-beta 1 protein production in retinoic acid-treated HL-60
cells: possible TGF-beta 1-mediated autocrine inhibition
LA Falk, F De Benedetti, N Lohrey, MC Birchenall-Roberts, LW Ellingsworth, CR Faltynek and FW Ruscetti
Biological Carcinogenesis and Development Program, Program Resources, Inc,
Dyn Corp, NCI-Frederick Cancer Research and Development Center, MD 21702.
Treatment of HL-60 cells, a human promyelocytic leukemia cell line, with
the vitamin A derivative retinoic acid (RA) for 7 days resulted in a
dose-dependent decrease in proliferation and increase in granulocytic
differentiation. The role of transforming growth factor-beta 1 (TGF- beta
1), a protein with pleiotropic effects on the proliferation and
differentiation of various cell types, was examined during RA-induced
differentiation of HL-60 cells. Although TGF-beta 1 alone had little effect
on proliferation or differentiation of HL-60 cells, addition of TGF-beta 1
to HL-60 cells treated with a suboptimum concentration of RA (1.0 nmol/L)
resulted in a marked decrease in proliferation with no effect on
granulocytic differentiation. Studies of the mechanism of RA- induced
TGF-beta sensitivity showed that although untreated HL-60 cells expressed
low levels of TGF-beta 1 binding proteins on the cell surface, the levels
were increased in a dose-dependent manner after RA treatment. Maximum
induction was achieved after treatment with 10 nmol/L RA and consisted
predominantly of the 65-Kd TGF-beta 1 receptor type. Moreover, RA treatment
also resulted in a dose-dependent increase in both TGF-beta 1 steady-state
mRNA expression and production of active TGF-beta with maximum induction at
10 nmol/LRA. RA treatment of HL-60 cells had no effect on TGF-beta 2 and
TGF-beta 3 mRNA expression. These data suggest that the effects of RA may
be mediated by a TGF-beta 1-mediated autocrine antiproliferative loop
during differentiation of HL-60 cells.
Volume 77,
Issue 6,
pp. 1248-1255,
03/15/1991
Copyright © 1991 by The American Society of Hematology
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