Bradykinin 2 receptor may stop glioma invasion

A laboratory version of a drug approved for use in Europe successfully stopped malignant brain-tumor cells from finding the blood vessels they need to thrive.

University of Alabama at Birmingham colleagues Vedrana Montana, PhD, and Harald Sontheimer, PhD, reported in The Journal of Neuroscience (2011;31[13]:4858-4867) that the signals attracting glioma cells to the blood vessels have been poorly understood. Now, however, the team has discovered that glioma cells use bradykinin—a peptide that increases the blood-vessel size—to find the vessels. Their research shows that glioma cells isolated from patient biopsies express bradykinin 2 receptors (B2R), and that bradykinin significantly enhances glioma cell migration and invasion. Montana and Sontheimer also learned that bradykinin acts as a chemoattractant, guiding glioma cells toward blood vessels in the brains of rats.

After introducing a B2R inhibitor known as HOE 140 to human glioma cells transplanted in a mouse model, the research team found that the agent bound to the B2R receptor on glioma cells. This interfered with the receptor's ability to bind to bradykinin and lead the cells to nourishing blood vessels. HOE 140 is a laboratory version of icatibant, a drug approved in Europe for the treatment of hereditary angioedema.

Before encountering HOE 140, 77% of glioma cells with bradykinin were able to locate a blood vessel and tap into its nutrients. Once the agent blocked the B2R receptors from interacting with bradykinin, however, only 19% of the glioma cells were able to find a blood vessel.

“These data strongly suggest that bradykinin, acting via B2R, acts as an important signal directing the invasion of glioma cells toward blood vessels,” concluded Montana and Sontheimer in their paper. “A clinically approved B2R antagonist is available that could be used as an anti-invasive drug in glioma patients in the future.”

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