"Regulation
of Runx Expression By Angiogenic Factors"
Annabelle Dando,
Biology, UMBC
1000 Hilltop Circle, Baltimore, MD 21250
Anthony Passaniti,
Ph.D. Pathology, University of Maryland, Greenebaum Cancer Center
Angiogenesis
rarely occurs in the body. It is a tightly regulated event and usually
is important for wound healing. Vascularization of tumors give cancer
a blood supply and allows for tumor growth and metastasis. Tumors, such
as breast cancer, activate angiogenesis through the
production of angiogeneic factors. To identify anti-angiogenic drugs,
it is necessary to identify which genes are activated by angiogenic factors
and regulate endothelial cell functions (such as proliferation, migration,
and differentiation).
Based on supporting research that Runx transcription factor is activated
by FGF and VEGF in murine endothelial cells and regulates cell migration
(Namba et al. 2000 Oncogene 19106-114) and that Runs is activated by IGF-1
in human bone marrow endothelial cells (Sun et al. 2001 Cancer Res 614994-5001),
it was hypothesized that treatment of endothelial
cells with the transcription factors VEGF and FGF would activate
expression of Runx 2.
HBME (human bone marrow endothelial cells), HMEC (human microdermal endothelial
cells), and UMEC (uterine microvascular endothelial cells) were each treated
with the transcription factors VEGF and FGF. After lysis of the cells
and RT-PCR, the samples were analyzed
for Runx 2 by agarose gel electrophoresis. The RNA samples of the HBME
cells were degraded and further improvements in RNA preparation will be
attempted. The HMEC cells did not show an increase of Runx expression
upon treatment with VEGF and FGF. The UMEC cells responded to VEGF and
FGF treatment with modest increases in Runx
expression.
