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J. Biol. Chem., Vol. 277, Issue 38, 35696-35702, September 20, 2002
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From the We have previously shown that CEACAM1, a
cell-adhesion molecule, acts as a tumor suppressor in prostate
carcinoma. Expression of CEACAM1 in prostate cancer cells suppresses
their growth in vivo. However, CEACAM1 has no effect on the
growth of prostate cancer cells in vitro. This difference
suggests that the antitumor effect of CEACAM1 may be due to
inhibition of tumor angiogenesis, perhaps by increased secretion of
antiangiogenic molecules from the cells. In this study, we have
demonstrated that expression of CEACAM1 in DU145 prostate cancer cells
induced the production of a factor or factors that specifically blocked
the growth of endothelial but not epithelial cells. Conditioned medium
from the CEACAM1-expressing cells but not control luciferase-expressing cells inhibited endothelial cell migration up a gradient of stimulatory vascular endothelial growth factor in vitro and inhibited
corneal neovascularization induced by basic fibroblast growth factor
in vivo. Moreover, conditioned medium from
CEACAM1-expressing cells induced endothelial cell apoptosis
in vitro. Only medium conditioned by CEACAM1 mutants that
were able to suppress tumor growth in vivo could cause
endothelial cell apoptosis. These observations suggest that
CEACAM1-mediated tumor suppression in vivo is, at least in
part, due to the ability of CEACAM1 to inhibit tumor angiogenesis.
Inhibition of Prostate Tumor Angiogenesis by the Tumor Suppressor
CEACAM1*
§,
,
Department of Microbiology-Immunology,
R. H. Lurie Cancer Center, Northwestern University Medical School,
Chicago, Illinois 60611 and the Departments of ¶ Molecular
Pathology, Neuro-oncology, and ** Genitourinary
Medical Oncology, The University of Texas M. D. Anderson Cancer
Center, Houston, Texas 77030
*
This work was supported by National Institutes of Health
Grants CA 64856 and CA 86342 (to S. H. L.), Core Grant CA 16672 (to the M. D. Anderson Cancer Center), Predoctoral Training Grant T32 CA
67759 (to V. T. E.), and an award from the Association for the Cure
of Cancer of the Prostate (CaPCURE) (to S. H. L.).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 Molecular
Pathology, Box 89, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030. Tel.: 713-794-1559; Fax: 713-794-4672; E-mail: slin@notes.mdacc.tmc.edu.
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