"Hot" Ingredient in Red Chili Pepper has Potent Anticancer Effects, Study Suggests
Apr 22, 2005 - 12:10:00 PM
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"Our results demonstrate that capsaicin is a potent anticancer agent, induces apoptosis in cancer cells and produces no significant damage to normal pancreatic cells, indicating its potential use as a novel chemotherapeutic agent for pancreatic cancer."
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By University of Pittsburgh Medical Center,
[RxPG] Two new studies suggest that vegetables such as broccoli and spices like red chili pepper, may provide a cancer-fighting benefit by slowing or preventing the growth of cancerous tumor cells.
The findings, being presented at the annual meeting of the American Association for Cancer Research held April 16 to 20 at the Anaheim Convention Center in Anaheim, Calif., looked at the effect of these dietary agents on cancers that have extremely poor prognoses despite advances in surgery and other therapies.
"In our studies, we decided to look at two particular cancers - ovarian and pancreatic - with low survival rates, to ascertain the contribution of diet and nutrition to the development of these cancers. We discovered that red chili pepper and broccoli appear to be effective inhibitors of the cancer process," said Sanjay K. Srivastava, Ph.D., lead investigator and assistant professor, department of pharmacology, University of Pittsburgh School of Medicine. "The contribution of diet and nutrition to cancer risk, prevention and treatment has been a major focus of research in recent years because certain nutrients in vegetables and dietary agents appear to protect the body against diseases such as cancer."
The first study, abstract number 2469, looked at the chemotherapeutic potential of capsaicin, the "hot" ingredient in red chili pepper that is often associated with antioxidative and anti-inflammatory activities, and found that it exhibited anticancer activity against pancreatic cancer cells.
Pancreatic cancer is one of the most aggressive cancers with an extremely poor prognosis. Dr. Srivastava and colleagues treated human pancreatic cells with capsaicin and found that it disrupted the mitochondrial function resulting in the release of cytochrome c, which induced apoptosis, or programmed cell death, in the cancerous cells without affecting normal pancreatic cells.
"Our results demonstrate that capsaicin is a potent anticancer agent, induces apoptosis in cancer cells and produces no significant damage to normal pancreatic cells, indicating its potential use as a novel chemotherapeutic agent for pancreatic cancer," said Dr. Srivastava.
In the second study, abstract number 5194, Dr. Srivastava and colleagues examined the therapeutic benefits of phenethyl isothiocyanate ( PEITC ), a constituent of cruciferous vegetables such as broccoli, on ovarian cancer.
Ovarian cancer, one of the leading causes of gynecologic cancer-related deaths among women in the United States, is often detected at an advanced stage, making it difficult to treat successfully. In the study, ovarian cancer cells were exposed to PEITC for 24 hours, which resulted in significant inhibition of the protein expression of epidermal growth factor receptor ( EGFR ).
EGFR plays a crucial role in the growth of ovarian cancer cells. PEITC treatment also inhibited the activation of Akt, which is responsible for protecting cancer cells against apoptosis. The concentrations of PEITC used in the study were at levels that may be achieved through dietary intake.
Publication:
The findings are presented at the annual meeting of the American Association for Cancer Research held April 16 to 20 at the Anaheim Convention Center in Anaheim, Calif
On the web:
www.upmc.edu 
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Additional information about the news article
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These studies were supported by a grant from the National Cancer Institute. Co-investigators include Sivakumar Loganathan, Ph.D., and Ian Humphreys, both with the department of pharmacology at the University of Pittsburgh School of Medicine.
Contact: Clare Collins
[email protected]
phone: ( 412 ) 647-3555
fax: ( 412 ) 624-3184
Lisa Rossi
[email protected]
phone: ( 412 ) 647-3555
fax: ( 412 ) 624-3184
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