Apoptosis

, Volume 11, Issue 1, pp 89–99

Induction of apoptosis in prostate tumor PC-3 cells and inhibition of xenograft prostate tumor growth by the vanilloid capsaicin

  • A. M. Sánchez
  • M. G. Sánchez
  • S. Malagarie-Cazenave
  • N. Olea
  • I. Díaz-Laviada
Article

DOI: 10.1007/s10495-005-3275-z

Cite this article as:
Sánchez, A.M., Sánchez, M.G., Malagarie-Cazenave, S. et al. Apoptosis (2006) 11: 89. doi:10.1007/s10495-005-3275-z

Abstract

Capsaicin, the pungent ingredient of hot chilli pepper, has been recently shown to induce apoptosis in several cell lines through a not well known mechanism. Here, we investigated the role of the vanilloid capsaicin in the death regulation of the human cancer androgen-resistant cell line PC-3. Capsaicin inhibited the growth of PC-3 with an IC50 of 20 μM cells and induced cell apoptosis, as assessed by flow cytometry and nuclei staining with DAPI. Capsaicin induced apoptosis in prostate cells by a mechanism involving reactive oxygen species generation, dissipation of the mitochondrial inner transmembrane potential (ΔΨm) and activation of caspase 3. Capsaicin-induced apoptosis was not reduced by the antagonist capsazepine in a dose range from 0.1 μM to 20 μM, suggesting a receptor-independent mechanism. To study the in vivo effects of capsaicinoids, PC-3 cells were grown as xenografts in nude mice. Subcutaneous injection of either capsaicin or capsazepine (5 mg/kg body weight) in nude mice suppressed PC-3 tumor growth in all tumors investigated and induced apoptosis of tumor cells. Our data show a role for capsaicin against androgen-independent prostate cancer cells in vitro and in vivo and suggest that capsaicin is a promising anti-tumor agent in hormone-refractory prostate cancer, which shows resistance to many chemotherapeutic agents.

Keywords

capsaicin capsazepine PC-3 cells prostate cancer vanilloids xenograft tumor 

Copyright information

© Springer Science + Business Media, Inc. 2006

Authors and Affiliations

  • A. M. Sánchez
    • 1
  • M. G. Sánchez
    • 1
  • S. Malagarie-Cazenave
    • 1
  • N. Olea
    • 1
  • I. Díaz-Laviada
    • 1
    • 2
  1. 1.Department of Biochemistry and Molecular Biology, School of MedicineUniversity of AlcaláMadridSpain
  2. 2.Departamento de Bioquímica y Biología Molecular, Facultad de MedicinaUniversidad de AlcaláMadridSpain

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