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Capsaicin Can Act as Co-Carcinogen, Study Finds; Chili Pepper Component Linked to Skin Cancer

Sep. 3, 2010 — A study in the journal Cancer Research by researchers at The Hormel Institute, University of Minnesota, links capsaicin, a component of chili peppers, to skin cancer. While the molecular mechanisms of the cancer-promoting effects of capsaicin are not clear and remain controversial, the new research has shown a definite connection to formation of skin cancer through various laboratory studies.


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Ann Bode, professor in the institute's Cellular and Molecular Biology Research Section, led the research team on this study along with colleagues Mun Kyung Hwang and Zigang Dong.

Capsaicin, widely consumed worldwide in foods that contain chili peppers, is also used in topical creams for pain relief and its role in cancer development is controversial. Capsaicin has been shown to induce apoptosis (cell death) in cancer cells. However, research findings have also shown that it can also act as a carcinogen, especially at the tumor promotion stage.

Bode says the possibility that capsaicin induces inflammation and may affect cancer development is a critical result of the study. "Most notably, the results raise concerns that a natural compound found in hot peppers used in over-the-counter topical pain remedies might increase skin cancer risk," Bode says.

The study's key findings include:

  • The co-carcinogenic effect of capsaicin appears to be mediated through the epidermal growth factor receptor (EGFR) and not the transient receptor potential vanilloid subfamily member 1 (TRPV1), a known pain receptor.
  • Topical application of capsaicin on the dorsal skin of wildtype or TRPV1 knockout mice induced tumors in both types but more and larger skin tumors in the knockout mice.
  • A known inflammatory enzyme, cyclooxygenase-2 (COX-2) was highly elevated following treatment with capsaicin.

Other researchers working with Bode on this study included Sanguine Byun, Nu Ry Song, Hyong Joo Lee and Ki Won Lee.

Funding for this research was provided by The Hormel Foundation, National Cancer Institute and the Korean Research Foundation.

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The above story is reprinted from materials provided by University of Minnesota.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Mun Kyung Hwang, Ann M. Bode, Sanguine Byun, Nu Ry Song, Hyong Joo Lee, Ki Won Lee, and Zigang Dong. Cocarcinogenic Effect of Capsaicin Involves Activation of EGFR Signaling but Not TRPV1. Cancer Research, 2010; 70 (17): 6859 DOI: 10.1158/0008-5472.CAN-09-4393
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