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Retinoic acid activates interferon regulatory factor-1 gene expression in
myeloid cells
S Matikainen, T Ronni, M Hurme, R Pine and I Julkunen
Molecular Biology Programme, National Public Health Institute, Helsinki,
Finland.
All-trans-retinoic acid (ATRA) is the drug of choice in the treatment of
acute promyelocytic leukemia (APL). ATRA induces both in vitro and in vivo
differentiation of APL cells into mature granulocytes. However, the
molecular mechanisms involved in ATRA-dependent growth inhibition and
cellular differentiation are not presently understood. The NB4 cell line,
which is derived from the bone marrow of a patient with APL during relapse,
can be used as a model system to study the growth and differentiation of
APL cells. Because interferon (IFN) regulatory factors (IRF-1 and IRF-2)
and other IFN-inducible gene products regulate cell growth, we analyzed the
effects of ATRA on the expression of these genes. We show that ATRA
directly activates IRF-1 gene expression, followed by activation of IRF-2
and 2'-5' oligoadenylate synthetase (OAS) gene expression with slower
kinetics. In addition to NB4 cells, ATRA also activated IRF-1 gene
expression in HL-60, U937, and THP-1 cells, which all respond to ATRA by
growth inhibition. A more than additive increase in IRF-1 gene expression
was seen with ATRA and IFN-gamma in NB4 cells. ATRA did not activate
nuclear factor kappa B or signal transducer and activator of transcription
(STAT) activation pathways, suggesting that an alternate mechanism is
involved in IRF-1 gene activation. The ATRA-induced expression of IRF-1, an
activator of transcription and repressor of transformation, may be one of
the molecular mechanisms of ATRA-induced growth inhibition, and the basis
for the synergistic actions of ATRA and IFNs in myeloid leukemia cells.
Volume 88,
Issue 1,
pp. 114-123,
07/01/1996
Copyright © 1996 by The American Society of Hematology
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