Treatment of the tumour-prone mice with capsaicin reduced tumour burden and extended the lifespans of the mice by over 30%.
The research, published this month in The Journal of Clinical Investigation, said the active ingredient produced chronic activation of a receptor, TRPV1, on cells lining the intestines of mice genetically modified to be TRPV1-deficient, which in turn triggered the reaction.
“Our data also suggested that TRPV1 triggering by dietary administration of capsaicin suppressed intestinal tumourigenesis,” the researchers said.
As a result they recommended the administration of TRPV1 agonists like capsaicin in combination with celecoxib, a COX-2 non-steroidal anti-inflammatory drug that treats some forms of arthritis and pain.
The receptor or ion channel TRPV1 was originally discovered in sensory neurons, where it acts as a guard against heat, acidity and chemicals in the environment. This latest research found that the receptor was also expressed by intestinal epithelial cells.
The scientists discovered that TRPV1 works as a tumor suppressor in the intestines through a “feedback loop” with the epidermal growth factor receptor (EGFR), reducing the risk of unwanted growth.
Dr Petrus de Jong, one of the study’s authors, said: "A basic level of EGFR activity is required to maintain the normal cell turnover in the gut. However, if EGFR signaling is left unrestrained, the risk of sporadic tumor development increases."
Professor Eyal Raz, another of the study’s authors, said: "Our data suggest that individuals at high risk of developing recurrent intestinal tumors may benefit from chronic TRPV1 activation.”
“We have provided proof-of-principle.”
Source: The Journal of Clinical Investigation
Published online ahead of print, doi:10.1172/JCI72340
“Ion channel TRPV1-dependent activation of PTP1B suppresses EGFR-associated intestinal tumorigenesis”
Authors: P.R. de Jong, N. Takahashi, A.R. Harris, J. Lee, S. Bertin,J. Jeffries, M. Jung, J. Duong, A.I. Triano, J. Lee, Y. Niv,D.S. Herdman, K. Taniguchi, C.W. Kim, H. Dong, L. Eckmann,S.M. Stanford, N. Bottini, M. Corr and E. Raz