Receptor may be cancer accomplice

A receptor protein that shows up on cancerous colon cells might serve as a new target for scientists seeking to derail this malignancy. A study in mice shows that shutting down the receptor slows cancer growth.

The receptor protein is called neuropilin-2 (NRP2). Earlier work hinted that it facilitates the activity of a family of proteins called vascular endothelial growth factors (VEGF), which dock onto other cell receptors. The VEGF proteins are best known for promoting signaling in blood vessel-lining cells that boost new vessel growth.

In the new study, researchers tested malignant and healthy cells taken from people with colon cancer. The cancerous cells typically produced NRP2 proteins, while nearby normal colon cells did not. Wiping out NRP2 receptors in malignant cells limited their survival in lab dish tests, says study coauthor Lee Ellis, a surgeon and cancer biologist at the M.D. Anderson Cancer Center in Houston.

When Ellis and his team implanted human colon tumors into mice, the tumors grew well and the cancer spread. But when the scientists implanted similar tumors, altered so they could not produce NRP2, the malignancies grew less and spawned fewer metastases. The work appears in the Jan. 16 Journal of the National Cancer Institute.

NRP2’s cancer-promoting actions remain somewhat mysterious. Although VEGF proteins are mainly thought to foster blood vessel growth, the effect that NRP2 has on VEGF in these cancerous colon cells might have more to do with abetting cancer cell growth directly than with vessel proliferation, Ellis says.

His team plans further tests. “We want to make sure this is truly a good target,” he says.

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