Abstract Title:

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

Abstract Source:

Hum Exp Toxicol. 2011 Oct ;30(10):1657-65. Epub 2011 Feb 7. PMID: 21300690

Abstract Author(s):

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

Article Affiliation:

1Department of Surgery, Changhua Christian Hospital, Changhua, Taiwan.


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 200μM 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 ofcapsaicin in clinical therapy could be useful for breast cancer patients.

Study Type : In Vitro Study

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