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J Biol Chem, Vol. 275, Issue 6, 4244-4250, February 11, 2000
From the Department of Physiology and Biomedical Engineering,
Norwegian University of Science and Technology,
N-7489 Trondheim, Norway
The CREM gene encodes both activators and
repressors of cAMP-induced transcription. Inducible cAMP early
repressor (ICER) isoforms are generated upon activation of an
alternative, intronic promoter within the CREM gene. ICER is proposed
to down-regulate both its own expression and the expression of other
genes that contain cAMP-responsive elements such as a number of growth
factors. Thus, ICER has been postulated to play a role in proliferation and differentiation. Here we show that ICER gene expression is induced
by gastrin, cholecystokinin (CCK), and epidermal growth factor in AR42J
cells. The time course of gastrin- and CCK-mediated ICER induction is
rapid and transient, similar to forskolin- and phorbol 12-myristate
13-acetate-induced ICER expression. The specific CCK-B receptor
antagonist L740,093 blocks the gastrin but not the CCK response,
indicating that both the CCK-B and the CCK-A receptor can mediate ICER
gene activation. Noteworthy, CREB is constitutively phosphorylated at
Ser-133 in AR42J cells, and ICER induction proceeds in the absence of
increased CREB Ser(P)-133. Gastrin-mediated ICER induction was not
reduced in the presence of the protein kinase A inhibitor H-89,
indicating a protein kinase A-independent mechanism. This is the first
report on ICER inducibility via Gq/G11
protein-coupled receptors.
Regulation of Inducible cAMP Early Repressor Expression by
Gastrin and Cholecystokinin in the Pancreatic Cell Line AR42J*
*
This work was supported by the Norwegian Cancer Society, The
Research Council of Norway, and the Cancer Foundation at the Trondheim
University Hospital.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 Physiology
and Biomedical Engineering, Norwegian University of Science and
Technology, Medisinsk Teknisk Senter, N-7005 Trondheim, Norway. Tel.:
47-73-59-86-16; Fax: 47-73-59-89-86; E-mail:
astridl@medisin.ntnu.no.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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