Embargoed Until: Thursday, October 30, 2014
Compound in Chili Pepper Slows
Lung Cancer Tumor Growth in Animal Study
New laboratory research shows capsaicin decreases growth of an aggressive form of lung cancer.
WASHINGTON, DC — Researchers presented new evidence today that capsaicin, the compound that gives chili peppers their heat, drives the death of lung cancer cells and slows tumor growth in mice.
The study was one of over 100 posters presented at the American Institute for Cancer Research (AICR) Annual Research Conference.
“Our studies have found that by giving the mice capsaicin in their food every day we are able to suppress lung tumors in mice models,” said Piyali Dasgupta, PhD, scientist at Marshall University and lead author of the studies.
The scientists focused on small cell lung cancer, a fast-growing type that makes up approximately 10 to 15 percent of lung cancers.
“We knew other lab studies had found capsaicin has anti-cancer activity but there was nothing on small cell lung cancer,” said Dasgupta. A paper by Dasgupta published this month finds that capsaicin degrades at a slower pace in the lung compared to other organs, such as the liver, kidney or in the blood. “This is good news because that means that there is more intact capsaicin in the lung, which is available to stop the growth of tumors.”
Using mice with an impaired immune system, the study induced tumor growth with human small cell lung cancer cells. Half the animals were fed capsaicin daily for six weeks. Compared to the mice eating standard food, the capsaicin-consuming animals showed decreased tumor growth. Further research in cell studies showed capsaicin caused the cancer cells to self-destruct, a process called apoptosis, but caused no harm to healthy lung cells.
One of the surprises of the study was that capsaicin did not use its typical receptor called the TRPV1, for causing the death of cancer cells. This TRPV1 receptor is responsible for the heat sensation we feel when we bite into a chili pepper. Another member of the TRPV family, TRPV6, was found responsible for the anti-cancer effect of capsaicin.
The amount of capsaicin the mice consumed was relatively mild, says Dasgupta, it had the hotness of a New Mexican pepper. Other research has established the amount used is considered safe, but research is only in the early stages.
“This research is important because we are working towards using capsaicin along with standard chemotherapeutic drugs to develop better combination therapies for patients with small cell lung cancer.”
The study was funded by the American Institute for Cancer Research.
- Find conference updates on Twitter at #AICR14.
- Read more news about the conference at aicr.org.
To the Editors:
- Rollyson WD, Stover CA, Brown KC, Perry HE, Stevenson CD, McNees CA, Ball JG, Valentovic MA, Dasgupta P. Bioavailability of capsaicin and its implications for drug delivery. J Control Release. 2014 Oct 11. [Epub ahead of print] Review.
- Lau JK, Brown KC, Dom AM, Witte TR, Thornhill BA, Crabtree CM, Perry HE, Brown JM, Ball JG, Creel RG, Damron CL, Rollyson WD, Stevenson CD, Hardman WE, Valentovic MA, Carpenter AB, Dasgupta P. Capsaicin induces apoptosis in human small cell lung cancer via the TRPV6 receptor and the calpain pathway. Apoptosis. 2014 Aug;19(8):1190-201.
The American Institute for Cancer Research (AICR) is the cancer charity that fosters research on the relationship of nutrition, physical activity and weight management to cancer risk, interprets the scientific literature and educates the public about the results. It has contributed over $105 million for innovative research conducted at universities, hospitals and research centers across the country. AICR has published two landmark reports that interpret the accumulated research in the field, and is committed to a process of continuous review. AICR also provides a wide range of educational programs to help millions of Americans learn to make dietary changes for lower cancer risk. AICR is a member of the World Cancer Research Fund International (WCRF).
Published on 12/31/2099
Published on 10/30/2014