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Vol. 59, Issue 4, 716-724, April 2001
1
Department of Experimental Toxicology, Medical Institute of
Environmental Hygiene at the Heinrich-Heine-University,
Düsseldorf, Germany (S.W., V.M., J.A.); and Division of Clinical
Pharmacology, Hospital for Sick Children, Toronto, Ontario, Canada
(P.A.H., J.M.Y.W., Y.W.)
Previous studies showed that TGF-
down-regulates aryl hydrocarbon
(AhR) expression in human lung carcinoma cells A549. Here we analyzed
the molecular mechanisms by which TGF- modulates AhR expression. A
5799-nucleotide 5'-flanking region of human AhR gene was isolated.
Transient transfection studies of full-length (hAhRP) and deletion
promoter constructs indicate the requirement of a
cis-regulatory element encompassing 
1980 to 1892 for
full constitutive activity. Basal hAhRP activity occurs in a
cell-specific manner; human hepatoma HepG2 cells possess a 10-fold
higher activity compared with A549 cells. TGF- exerts cell-specific
effects on hAhRP activity. Treatment of cells with 100 pM TGF- leads
to a 50% inhibition in A549 and a 3-fold induction in HepG2 cells. Deletion mutagenesis identified a TGF--responsive sequence
containing a functional conserved Smad-binding element. Transient
overexpression of Smad 2, 3, and 4 indicates that these signal
transducers modulate hAhRP activity. The down-regulation of AhR by
TGF- is modulated by 5'-TG-3'-interacting factor (TGIF). Transient
overexpression of TGIF in MDA-MB231 and HepG2 cells led to inhibition
of hAhRP activity and a similar decrease of AhR mRNA expression. Our
findings indicate that Smad proteins are involved in the cell-specific regulation of AhR expression by TGF-.
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