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Vol. 292, Issue 1, 31-37, January 2000
Medicine Branch, Division of Clinical Sciences, National Cancer
Institute, National Institutes of Health, Bethesda, Maryland
The induction of angiogenesis is known to play a critical role in the
successful growth, invasion, and metastasis of a tumor. A tumor will
not grow beyond a few cubic millimeters without the formation of its
own capillary network. Several antiangiogenic agents are under
investigation in the clinic setting for the treatment of cancer.
Carboxyamido-triazole (CAI), an inhibitor of Ca2+-mediated
signal transduction, has been previously shown to inhibit angiogenesis
in vitro and in vivo and to down-regulate matrix metalloproteinase-2 in
vitro. Diminished levels of intracellular Ca2+ result in
decreased nitric-oxide synthase (NOS) activity and thereby inhibit the
production and release of NO. The antiangiogenic activity of CAI was
investigated by assessing microvessel growth from rat aortic segments
and in cell culture using human aortic endothelial cells (HAECs). With
these models, vascular endothelial growth factor (VEGF) and NOS
production and secretion were evaluated. CAI concentrations ranging
from 0.25 to 12.0 µg/ml inhibited new microvessel formation in rat
aortic cultures and HAEC proliferation in a dose-dependent manner.
Additionally, HAECs treated with CAI showed a dose-dependent decrease
of NOS expression and a decrease in both VEGF expression and secretion.
Rat aortic segments demonstrated decreased VEGF expression in situ on
immunostaining. These data suggest that modulation of the NOS-NO-VEGF
pathway through Ca2+-mediated signaling by CAI inhibits
angiogenesis in vitro.
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