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Cancer Research
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About the Cover

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Capsaicin is a principal pungent ingredient in hot peppers, which are consumed worldwide. Capsaicin has been shown to induce cancer cell death, and it has also been suggested that capsaicin may act as a carcinogen or cocarcinogen during the promotion stage of cancer. Hwang and colleagues show that capsaicin has a cocarcinogenic effect on TPA-promoted skin carcinogenesis in vivo that is mediated through the epidermal growth factor receptor (EGFR) and not the transient receptor potential vanilloid subfamily member 1 (TRPV1). Significantly, topical application of capsaicin on the dorsal skin of wild-type or TRPV1 knockout mice induced more and larger skin tumors in the knockout mice, suggesting that capsaicin acts through a TRPV1-independent mechanism. Notably, cyclooxygenase-2 (COX-2) expression was highly elevated with capsaicin treatment in TRPV1 knockout mice, and inhibitors of EGFR/MEK signaling suppressed capsaicin/TPA-induced COX-2 expression. These results raise concerns that a natural compound found in hot peppers used in over-the-counter topical pain remedies may heighten skin cancer risk by affecting EGFR-dependent signaling. For details, see the article by Hwang and colleagues on page 6859 of this issue.

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Cancer Research: 70 (17)
September 2010
Volume 70, Issue 17
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Issue Highlights

  • Voltage-Gated Na+ Channel SCN5A Is a Key Regulator of a Gene Transcriptional Network That Controls Colon Cancer Invasion
  • PIK3CA Mutation Uncouples Tumor Growth and Cyclin D1 Regulation from MEK/ERK and Mutant KRAS Signaling
  • Cocarcinogenic Effect of Capsaicin Involves Activation of EGFR Signaling but Not TRPV1
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Copyright © 2021 by the American Association for Cancer Research.

Cancer Research Online ISSN: 1538-7445
Cancer Research Print ISSN: 0008-5472
Journal of Cancer Research ISSN: 0099-7013
American Journal of Cancer ISSN: 0099-7374

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