SciSign: Cancer-Associated Protein BRAF Identified as a Potential Driver of Chronic Pain

Researchers at the University of Texas MD Anderson Cancer Center have identified a protein that may play a key role in the development and persistence of chronic pain following nerve injury. The protein, BRAF, is already well known for its role in the development of certain types of cancer. The findings were published in Science Signaling (SciSign).

The researchers focused on neuropathic pain, a condition that develops after nerve damage and can persist for a prolonged period. This type of pain is often difficult to treat with conventional painkillers.

The study found that after a nerve is injured, BRAF moves from peripheral nerve cells toward their endings in the spinal cord. There, it activates signaling processes that enhance the activity of NMDA receptors. These protein structures are involved in transmitting signals between nerve cells, and excessive NMDA receptor activity can intensify pain.

When the researchers blocked BRAF using vemurafenib, the animals became less sensitive to touch, pressure and heat. A similar effect was observed when the scientists used selumetinib, which blocks the MEK signaling pathway associated with BRAF. Importantly, the treatments did not alter normal sensitivity in animals without nerve damage.

Additional experiments further confirmed BRAF’s role. Removing the Braf gene reduced chronic pain sensitivity, while artificially activating BRAF caused increased sensitivity even in the absence of nerve injury.

According to the researchers, the findings raise the possibility of repurposing existing cancer drugs to treat neuropathic pain. However, the results have so far been obtained only in preclinical models. Further studies will be needed to determine appropriate doses, effective drug-delivery methods and potential side effects before the approach can be tested in humans.

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