A spicy chemical may be able to slow down or reduce gut tumors, according to a recent study.

Researchers from the University of California, San Diego School of Medicine found that dietary capsaicin - the active ingredient in chili peppers - produces chronic activation of a receptor on cells lining the intestines of mice, triggering a reaction that ultimately reduces the risk of colorectal tumors.

The receptor or ion channel, called TRPV1, was originally discovered in sensory neurons, where it acts as a sentinel for heat, acidity and spicy chemicals in the environment.

"These are all potentially harmful stimuli to cells," said Eyal Raz, senior author of the study. "Thus, TRPV1 was quickly described as a molecular 'pain receptor.' This can be considered to be its conventional function, which all takes place in the nervous system."

However, researchers found that TPRV1 is also expressed by cells of the intestines, where it is activated by epidermal growth factor receptor -- an important driver of cell proliferation in the intestines, whose epithelial lining is replaced approximately every four to six days.

"A basic level of EGFR activity is required to maintain the normal cell turnover in the gut," said Petrus de Jong, MD, first author of the study. "However, if EGFR signaling is left unrestrained, the risk of sporadic tumor development increases."

The scientists discovered that TRPV1, once activated by the EGFR, initiates a direct negative feedback on the EGFR, dampening the latter to reduce the risk of unwanted growth and intestinal tumor development. They found that mice genetically modified to be TRPV1-deficient suffered higher-than-normal rates of intestinal tumor growths.

Based on their findings, epithelial TRPV1 normally works as a tumor suppressor in the intestines.

In addition, molecular studies of human colorectal cancer samples recently uncovered multiple mutations in the TRPV1 gene, though Raz noted that currently there is no direct evidence that TRPV1 deficiency is a risk factor for colorectal cancer in humans.

"A direct association between TRPV1 function and human colorectal cancer should be addressed in future clinical studies," de Jong said.

The findings were recently published in The Journal of Clinical Investigation