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Capsaicin, a Component of Red Peppers, Inhibits the Growth of Androgen-Independent, p53 Mutant Prostate Cancer Cells

¹ Division of Hematology/Oncology, Cedars-Sinai Medical Center, University of California at Los Angeles School of Medicine; ² Department of Radiation Oncology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California; and ³ Division of Hematology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan

Requests for reprints: Sören Lehmann, Cedars-Sinai Medical Center/University of California at Los Angeles School of Medicine, 8700 Beverly Boulevard, Los Angeles, CA 90048. Phone: 310-423-7758; Fax: 310-423-0225; E-mail: LehmannS{at}cshs.org.

Capsaicin is the major pungent ingredient in red peppers. Here, we report that it has a profound antiproliferative effect on prostate cancer cells, inducing the apoptosis of both androgen receptor (AR)-positive (LNCaP) and -negative (PC-3, DU-145) prostate cancer cell lines associated with an increase of p53, p21, and Bax. Capsaicin down-regulated the expression of not only prostate-specific antigen (PSA) but also AR. Promoter assays showed that capsaicin inhibited the ability of dihydrotestosterone to activate the PSA promoter/enhancer even in the presence of exogenous AR in LNCaP cells, suggesting that capsaicin inhibited the transcription of PSA not only via down-regulation of expression of AR, but also by a direct inhibitory effect on PSA transcription. Capsaicin inhibited NF- activation by preventing its nuclear migration. In further studies, capsaicin inhibited tumor necrosis factor-–stimulated degradation of IB in PC-3 cells, which was associated with the inhibition of proteasome activity. Taken together, capsaicin inhibits proteasome activity which suppressed the degradation of IB, preventing the activation of NF-B. Capsaicin, when given orally, significantly slowed the growth of PC-3 prostate cancer xenografts as measured by size [75 ± 35 versus 336 ± 123 mm³ (±SD); P = 0.017] and weight [203 ± 41 versus 373 ± 52 mg (±SD); P = 0.0006; capsaicin-treated versus vehicle-treated mice, respectively]. In summary, our data suggests that capsaicin, or a related analogue, may have a role in the management of prostate cancer. (Cancer Res 2006; 66(6): 3222-9)

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