Dietary capsaicin - an 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 tumours.
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, professor of Medicine at the University of California, San Diego School of Medicine.
But Raz and colleagues have found that TPRV1 is also expressed by epithelial cells of the intestines, where it is activated by epidermal growth factor receptor or EGFR.
EGFR is 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, first author of the study.
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 tumour development.
They found that mice genetically modified to be TRPV1-deficient suffered higher-than-normal rates of intestinal tumour growths.
"These results showed us that epithelial TRPV1 normally works as a tumour suppressor in the intestines," said de Jong.
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.
But if such proves to be the case, the current study suggests one potential remedy might be spicy capsaicin, which acts as an irritant in mammals, generating a burning sensation in contact with tissue.
The finding was published in The Journal of Clinical Investigation.
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