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Autocrine loop through cholecystokinin-B/gastrin receptors involved in
growth of human leukemia cells
N Iwata, T Murayama, Y Matsumori, M Ito, A Nagata, T Taniguchi, K Chihara, Y Matsuo, J Minowada and T Matsui
Department of Medicine, Kobe University School of Medicine, Japan.
The cholecystokinin (CCK)-B/gastrin receptor binds two brain-gut hormones,
CCK and gastrin, with high affinities. These peptides have a trophic effect
on gastrointestinal cells expressing the receptor in vivo as well as in
vitro. Recently, this receptor mRNA was reported to be expressed in
immunocytes localized in the lamina propria of normal rat stomach mucosa.
Here, we studied the receptor expression in human hematopoietic cells in
order to determine whether they play a role in cell growth. The
CCK-B/gastrin receptor mRNA was detectable in the polymorphonuclear (PMN)
cells but not in the mononuclear cells of normal peripheral white blood
cells by reverse transcription-polymerase chain reaction. The receptor
transcript was, however, expressed in human leukemia cell lines (14 of 18
cell lines tested) derived from not only myeloid, but also T- and B-
lymphoid lineages. The CCK-B/gastrin receptors on several leukemia cell
lines were shown to be biologically active by demonstrating
ligand-dependent cell proliferation in serum- deprived medium.
Interestingly, a human CCK-B/gastrin receptor specific antagonist, YM022,
but not its stereotype isoform, selectively inhibited the DNA synthesis of
THP-1, MOLT-16, MOLT-14, and CCRF-CEM in the absence of exogenous peptide
ligands. Further investigation revealed that these leukemia cell lines and
normal PMN cells also expressed gastrin mRNA. These results suggest that
growth of human leukemia cells is promoted by an autocrine mechanism
through the CCK- B/gastrin receptors.
Volume 88,
Issue 7,
pp. 2683-2689,
10/01/1996
Copyright © 1996 by The American Society of Hematology
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