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J. Biol. Chem., Vol. 275, Issue 43, 33929-33936, October 27, 2000
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From the The MUC4 mucin is considered as the
homologue of rat sialomucin complex (SMC, rat Muc4) due to its similar
structural organization. Like SMC, MUC4 may also exist as two subunits:
a mucin type unit known as MUC4
Retinoic Acid-dependent Transforming Growth
Factor-
2-mediated Induction of MUC4 Mucin Expression in
Human Pancreatic Tumor Cells Follows Retinoic Acid Receptor-
Signaling Pathway*
,,,
Department of Biochemistry and Molecular
Biology and Eppley Institute for Research in Cancer and Allied Diseases
and § Department of Pathology and Microbiology, University
of Nebraska Medical Center, Omaha, Nebraska 68198 and ¶ Unite 377 INSERM, Place de Verdun, 59045 Lille Cedex, France
and a growth factor-like
transmembrane subunit, MUC4
. The expression of MUC4 in
normal human pancreas is not detectable, but it is highly expressed in
pancreatic tumor cells. In the present study, we investigated the
regulation of MUC4 expression in human pancreatic tumor cells
CD18/HPAF, exhibiting a high level of MUC4 transcripts and
protein. When these cells were adapted to grow in the serum-free medium
(CD18/HPAF-SF), the MUC4 expression was undetectable. Among several
serum constituents, all-trans-retinoic acid (RA) induced
the expression of MUC4 transcripts in a concentration- and
time-dependent manner. The RA-mediated increase in the
level of the MUC4 transcript coincided with an increased
expression of transforming growth factor-2
(TGF-2) transcript. The antagonist of the
retinoic acid receptor (RAR)- (Ro41-5253) abrogated the expression
of MUC4 and TGF-2 induced by RA.
The exogenous addition of TGF-2 also increased the MUC4
expression. The TGF--neutralizing antibody blocked the
RA-induced as well as TGF-2-mediated MUC4 expression. In
conclusion, induction of MUC4 expression in pancreatic carcinoma by RA is mediated through the RAR- signaling pathway, and
TGF-2 may serve as an interim mediator of this regulated expression.
*
This work was supported by National Institutes of Health
Grants CA 78590 (to S. K. B) and CA72781 (to R. K. S).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of
Biochemistry and Molecular Biology, 984525 Nebraska Medical Center,
Omaha, NE 68198-4525. Tel.: 402-559-5455; Fax: 402-559-6650; E-mail: sbatra@unmc.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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