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Blood, 15 November 2000, Vol. 96, No. 10, pp. 3529-3536
NEOPLASIA
Differentiation-independent retinoid induction of folate receptor
type  , a potential tumor target in myeloid leukemia
Hui Wang,
Xuan Zheng,
Frederick G. Behm, and
Manohar Ratnam
From the Department of Biochemistry and Molecular
Biology, Medical College of Ohio, Toledo, OH, and the Department of
Immunopathology, St. Jude's Children's Research Hospital, Memphis,
TN.
Folate receptor (FR) type  is expressed in the myelomonocytic
lineage, predominantly during neutrophil maturation and in myeloid
leukemias. FR- expression was elevated up to 20-fold by
all-trans retinoic acid (ATRA) in KG-1 myeloid leukemia
cells in a dose-dependent and reversible manner in the absence of
terminal differentiation or cell growth inhibition. ATRA also increased FR- expression in vitro in myeloid leukemia cells from patient marrow. FR- was not up-regulated in KG-1 cells treated with phorbol ester, dexamethasone, 1,25-dihydroxy vitamin D3, or
transforming growth factor . ATRA did not induce FR- expression
in receptor negative cells of diverse origin. The ATRA-induced increase
in FR- expression in KG-1 cells occurred at the level of messenger RNA synthesis, and in 293 cells containing a stably integrated FR-
promoter-luciferase reporter construct, ATRA induced expression of the
reporter. From experiments using retinoid agonists and antagonists and
from cotransfection studies using the FR- promoter and expression
plasmids for the nuclear receptors retinoic acid receptor
(RAR) , RAR, or RAR , it appears that the retinoid
effect on FR- expression could be mediated by ligand binding to RARs , , or , but not to retinoid X receptors.
Furthermore, there was apparent cross-talk between RAR and RAR
selective agonists or antagonists, suggesting a common downstream
target for RAR isoforms in inducing FR- expression. Thus,
blocks in the RAR-specific pathway of retinoid-induced
differentiation may be bypassed during retinoid induction of FR-
expression. The results suggest that to facilitate FR-targeted
therapies, retinoids may be used to modulate FR- expression in
myeloid leukemia cells refractory to retinoid differentiation therapy.
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