Cleveland Clinic researchers have discovered a protein that inhibits the growth of cancerous tumors and slows development of new blood vessels that help cancers to spread.
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The creation of new blood vessels, or angiogenesis, plays a critical role in the growth of cancer and its spread through the body.
The new blood vessels deliver nutrients and oxygen to the cancer tumor. This allows the tumor to survive, expand and travel to other parts of the body.
Because tumors cannot grow beyond a certain size or spread without a blood supply, scientists are trying to find ways to block tumor angiogenesis, says the National Institutes of Health (NIH).
A family of proteins called vascular endothelial growth factors (VEGFs) is behind angiogenesis. One protein, called VEGF-A, is the principal driver of the process.
A research team led by Paul Fox, PhD, of the Department of Cellular and Molecular Medicine in Cleveland Clinic’s Lerner Research Institute, discovered that a variant of VEGF-A decreases angiogenesis.
The researchers named the variant VEGF-Ax. The protein cuts off the blood supply to tumors and inhibits tumor development in animal models.
The research has the potential to pave the way for further scientific inquiry, Dr. Fox says.
“This research is significant because it will open new avenues of angiogenesis and cancer research,” Dr. Fox says.
Possible future benefits
Patients may see benefits as well, Dr. Fox says.
“It is important for patients as it could potentially lead to new diagnostic tools and improved treatments to reduce the spread of cancer.” Dr. Fox says.
VEGF-Ax is 22 amino acids longer than VEGF-A. The newly discovered protein forms when the ribosome – the cellular machinery that translates genes (actually messenger RNAs) into proteins – “reads” through its genetic stop sign.
“It is truly remarkable that a small change in a protein sequence leads not just to a protein with a different function, but one with a function completely opposite to the original,” Dr, Fox says. “In the context of cancer, the small extension changes a very ‘bad’ protein into a very ‘good’ one.”
The research, which was supported by NIH grants, appears today in the journal Cell.
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