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Blood, Vol. 94 No. 12 (December 15), 1999:
pp. 4233-4246
The BCR/ABL Oncogene Alters the Chemotactic Response to
Stromal-Derived Factor-1
Ravi Salgia,
Elizabeth Quackenbush,
Jeffrey Lin,
Natalia Souchkova,
Martin Sattler,
Darren S. Ewaniuk,
Kevin M. Klucher,
George Q. Daley,
Stine K. Kraeft,
Robert Sackstein,
Edwin P. Alyea III,
Ulrich H. von Andrian,
Lan Bo Chen,
Jose-Carlos Gutierrez-Ramos,
Ann-Marie Pendergast, and
James D. Griffin
From the Department of Medical Oncology and Division of Hematologic
Oncology, Division of Cellular and Molecular Biology, Dana-Farber
Cancer Institute, Harvard Medical School, Boston, MA; Center for Blood
Research and Harvard Medical School, Boston, MA; The
Children's Hospital, Boston, MA; Whitehead Institute Biomedical
Research, Cambridge, MA; Department of Pharmacology and Cancer Biology,
Duke University Medical Center, Levine Science Research Center, Durham,
NC; Millennium Pharmaceuticals Inc, Cambridge, MA; and Department of
Medicine, Brigham and Women's Hospital/Massachusetts General Hospital,
Boston, MA.
The chemokine stromal-derived factor-1 (SDF-1) is a
chemoattractant for CD34+ progenitor cells, in vitro and
in vivo. The receptor for SDF-1, CXCR-4, is a 7 transmembrane domain
receptor, which is also a coreceptor for human immunodeficiency virus
(HIV). Here we show that transformation of hematopoietic cell lines by
BCR/ABL significantly impairs their response to SDF-1. Three
different hematopoietic cell lines, Ba/F3, 32Dcl3, and Mo7e, were found
to express CXCR-4 and to respond to SDF-1 with increased migration
in a transwell assay. In contrast, after transformation by the BCR/ABL
oncogene, the chemotactic response to SDF-1 was reduced in all 3 lines. This effect was directly due to BCR/ABL, because Ba/F3 cells, in
which the expression of BCR/ABL could be regulated by a
tetracycline-inducible promoter, also had reduced chemotaxis to
SDF-1 when BCR/ABL was induced. The reduced response to SDF-1 was
not due to an inability of BCR/ABL-transformed cell lines to migrate in
general, as spontaneous motility of BCR/ABL-transformed cells was
increased. In mice, injection of SDF-1 into the spleen resulted in a
transient accumulation of untransformed Ba/F3 cells, but not
Ba/F3.p210BCR/ABL cells administered simultaneously. The
mechanism may involve inhibition of CXCR-4 receptor function, because
in BCR/ABL-transformed cells, CXCR-4 receptors were expressed on the
cell surface, but SDF-1 calcium flux was inhibited. Because SDF-1
and CXCR-4 are felt to be involved in progenitor cell homing to marrow,
the abnormality decribed here could contribute to the homing and
retention defects typical of immature myeloid cells in chronic
myelogenous leukemia.
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