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Article

Diallyl trisulfide induces apoptosis in human primary colorectal cancer cells

  • Authors:
    • Chun-Shu Yu
    • An-Cheng Huang
    • Kuang-Chi Lai
    • Yi-Ping Huang
    • Meng-Wei Lin
    • Jai-Sing Yang
    • Jing-Gung Chung
  • View Affiliations / Copyright

    Affiliations: School of Pharmacy, China Medical University, Taichung 404, Taiwan, R.O.C., Department of Nursing, St. Mary's Medicine Nursing and Management College, Yilan 266, Taiwan, R.O.C., School of Medicine, China Medical University, Taichung 404, Taiwan, R.O.C., Department of Physiology, China Medical University, Taichung 404, Taiwan, R.O.C., Department of Biological Science and Technology, China Medical University, Taichung 404, Taiwan, R.O.C., Department of Pharmacology, China Medical University, Taichung 404, Taiwan, R.O.C.
  • Pages: 949-954
    |
    Published online on: June 20, 2012
       https://doi.org/10.3892/or.2012.1882
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Abstract

Colorectal cancer (CRC) is one of the most prevalent types of cancer worldwide and a common cause of morbidity and mortality in humans. The garlic-derived organosulfur compound diallyl trisulfide (DATS) has been shown to induce apoptosis in many human cancer cell lines in vitro and also affords significant protection against cancer in animal tumor models in vivo. There is no available information to show DATS-induced apoptosis in vitro and the molecular mechanisms of apoptosis in human primary colorectal cancer cells. In this study, we investigated the cytotoxic effects in DATS in primary colorectal cancer cells. DATS inhibited the viability of primary colorectal cancer cells in a time- and dose-dependent manner. After treatment with DATS, primary colorectal cancer cells exhibited DNA condensation by DAPI stain. DATS increased reactive oxygen species (ROS) production in primary colorectal cancer cells. The mitochondria-dependent apoptotic signaling pathway was shown to be involved as determined by increase in the levels of cytochrome c, Apaf-1, AIF and caspase-3 and caspase-9 in DATS-treated primary colorectal cancer cells. The decrease in the level of ΔΨm was associated with an increase in the Bax/Bcl-2 ratio which led to activation of caspase-9 and -3. Based on our results, DATS induces apoptotic cell death in human primary colorectal cancer cells through a mitochondria-dependent signaling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Yu C, Huang A, Lai K, Huang Y, Lin M, Yang J and Chung J: Diallyl trisulfide induces apoptosis in human primary colorectal cancer cells. Oncol Rep 28: 949-954, 2012.
APA
Yu, C., Huang, A., Lai, K., Huang, Y., Lin, M., Yang, J., & Chung, J. (2012). Diallyl trisulfide induces apoptosis in human primary colorectal cancer cells. Oncology Reports, 28, 949-954. https://doi.org/10.3892/or.2012.1882
MLA
Yu, C., Huang, A., Lai, K., Huang, Y., Lin, M., Yang, J., Chung, J."Diallyl trisulfide induces apoptosis in human primary colorectal cancer cells". Oncology Reports 28.3 (2012): 949-954.
Chicago
Yu, C., Huang, A., Lai, K., Huang, Y., Lin, M., Yang, J., Chung, J."Diallyl trisulfide induces apoptosis in human primary colorectal cancer cells". Oncology Reports 28, no. 3 (2012): 949-954. https://doi.org/10.3892/or.2012.1882
Copy and paste a formatted citation
x
Spandidos Publications style
Yu C, Huang A, Lai K, Huang Y, Lin M, Yang J and Chung J: Diallyl trisulfide induces apoptosis in human primary colorectal cancer cells. Oncol Rep 28: 949-954, 2012.
APA
Yu, C., Huang, A., Lai, K., Huang, Y., Lin, M., Yang, J., & Chung, J. (2012). Diallyl trisulfide induces apoptosis in human primary colorectal cancer cells. Oncology Reports, 28, 949-954. https://doi.org/10.3892/or.2012.1882
MLA
Yu, C., Huang, A., Lai, K., Huang, Y., Lin, M., Yang, J., Chung, J."Diallyl trisulfide induces apoptosis in human primary colorectal cancer cells". Oncology Reports 28.3 (2012): 949-954.
Chicago
Yu, C., Huang, A., Lai, K., Huang, Y., Lin, M., Yang, J., Chung, J."Diallyl trisulfide induces apoptosis in human primary colorectal cancer cells". Oncology Reports 28, no. 3 (2012): 949-954. https://doi.org/10.3892/or.2012.1882
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