A study led by researchers at Boston University School of Medicine
(BUSM) demonstrates a new mechanism involving a signaling protein and
its receptor that may block the formation of new blood vessels and
cancer growth. The findings are published in the December issue of Science Signaling.
gnaling protein produced by damaged cells, which binds to one of its
receptors VEGFR-2, located on the surface of blood vessel cells. Once
VEGF is bound to its receptor, it is activated and sends a biochemical
signal to the inside of the blood vessel cell to initiate angiogenesis.
There are currently multiple Federal Drug Administration-approved
medications that target this process. However these medications are
limited by insufficient efficacy and the development of resistance.
The researchers demonstrated that a biochemical process called
methylation, which can regulate gene expression, also affects VEGFR-2,
and this can lead to angiogenesis. Using multiple methods, the
researchers were able to interfere with the methylation process of
VEGFR-2 and subsequently block angiogenesis and tumor growth.
"The study points to the methylation of VEGFR-2 as an exciting, yet
unexplored drug target for cancer and ocular angiogenesis, ushering in a
new paradigm in anti-angiogenesis therapy," said Nader Rahimi, PhD,
associate professor of pathology, BUSM, who served as the study's senior
investigator.
Story Source:
The above story is based on materials provided by Boston University Medical Center, via EurekAlert!, a service of AAAS.
Courtesy: ScienceDaily
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