Capsaicin may induce breast cancer cell death through apoptosis-inducing factor involving mitochondrial dysfunction

H. C. Chang, S. T. Chen, S. Y. Chien, S. J. Kuo, H. T. Tsai, D. R. Chen

Research output: Contribution to journalArticlepeer-review

60 Citations (Scopus)


The majority of breast cancer patients are resistant to chemotherapy or radiotherapy due to the down-regulation or lack of caspase-3 expression. Capsaicin was found to inhibit cancer cell growth in caspase-3-deficient human breast cancer cells. This study aimed to investigate the growth-inhibitive effect of capsaicin and its mechanisms in human breast cancer cell lines, MCF-7 and BT-20. The results showed that cell viability decreased in a dose-dependent manner in both the caspase-3-deficient and non-deficient cells through inducing cell apoptosis and arresting the cell cycle in the S phase. Capsaicin significantly decreased mitochondria membrane potential, induced the cleavage of PARP-1, and decreased procaspase-7 expression in both cells. Apoptosis-inducing factor (AIF) was distinctly released from mitochondria and translocated into the cytoplasm and nucleus in MCF-7 cells (52.9%), but not in BT-20 cells (2%) after treatment with 200 μM of capsaicin for 24 hours. Capsaicin inhibited breast cancer cell growth through inducing cell apoptosis and cell cycle arrest in the S phase. This apoptotic effect could be induced through the mitochondrial pathway, and PARP-1 subsequently cleaved by activation of caspase-7. The application of capsaicin in clinical therapy could be useful for breast cancer patients.

Original languageEnglish
Pages (from-to)1657-1665
Number of pages9
JournalHuman and Experimental Toxicology
Issue number10
Publication statusPublished - Oct 2011
Externally publishedYes


  • apoptosis-inducing factor
  • breast cancer cells
  • capsaicin
  • caspase-independent pathway
  • mitochondrial dysfunction

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis


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