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Article

Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway

  • Authors:
    • Chao-Ying Lee
    • Yung-Shin Chien
    • Tai-Hui Chiu
    • Wen-Wen Huang
    • Chi-Cheng Lu
    • Jo-Hua Chiang
    • Jai-Sing Yang
  • View Affiliations / Copyright

    Affiliations: School of Pharmacy, China Medical University, Taichung, Taiwan, R.O.C., Department of Pharmacology, China Medical University, Taichung, Taiwan, R.O.C., Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, R.O.C., Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan, R.O.C.
  • Pages: 1883-1888
    |
    Published online on: August 30, 2012
       https://doi.org/10.3892/or.2012.2000
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Abstract

Vitexin, a lignan compound, has been shown to exert apoptotic actions on human breast cancer cell lines and to have anti-inflammatory activities. Nevertheless, there is currently no study addressing the effects of vitexin on the induction of apoptosis in U937 human leukemia cells. The aim of this study was to determine the anticancer effects and molecular mechanisms of vitexin on U937 leukemia cells. We showed that vitexin can potently induce programmed cell death in U937 leukemia cell growth as well as morphological changes that were examined by MTT assay and phase contrast microscopy, respectively. The DNA content and the levels of mitochondrial membrane potential (∆Ψm) were determined by flow cytometric analysis. The cell cycle arrest-regulated and apoptosis-associated protein levels were measured by western blotting. Vitexin-triggered apoptosis was accompanied by a decrease of the level of ∆Ψm and the percentage of viability and provoked apoptosis in U937 cells. The downregulation of the protein level for Bcl-2 with the simultaneous upregulation of caspase-3 and -9 protein expression in U937 cells were observed after treatment with vitexin. Therefore, our data provide a potential mechanism for the chemopreventive activity of vitexin, and we suggest that vitexin may serve as a therapeutic agent for the treatment of human leukemia.
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Copy and paste a formatted citation
Spandidos Publications style
Lee C, Chien Y, Chiu T, Huang W, Lu C, Chiang J and Yang J: Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway. Oncol Rep 28: 1883-1888, 2012.
APA
Lee, C., Chien, Y., Chiu, T., Huang, W., Lu, C., Chiang, J., & Yang, J. (2012). Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway. Oncology Reports, 28, 1883-1888. https://doi.org/10.3892/or.2012.2000
MLA
Lee, C., Chien, Y., Chiu, T., Huang, W., Lu, C., Chiang, J., Yang, J."Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway". Oncology Reports 28.5 (2012): 1883-1888.
Chicago
Lee, C., Chien, Y., Chiu, T., Huang, W., Lu, C., Chiang, J., Yang, J."Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway". Oncology Reports 28, no. 5 (2012): 1883-1888. https://doi.org/10.3892/or.2012.2000
Copy and paste a formatted citation
x
Spandidos Publications style
Lee C, Chien Y, Chiu T, Huang W, Lu C, Chiang J and Yang J: Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway. Oncol Rep 28: 1883-1888, 2012.
APA
Lee, C., Chien, Y., Chiu, T., Huang, W., Lu, C., Chiang, J., & Yang, J. (2012). Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway. Oncology Reports, 28, 1883-1888. https://doi.org/10.3892/or.2012.2000
MLA
Lee, C., Chien, Y., Chiu, T., Huang, W., Lu, C., Chiang, J., Yang, J."Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway". Oncology Reports 28.5 (2012): 1883-1888.
Chicago
Lee, C., Chien, Y., Chiu, T., Huang, W., Lu, C., Chiang, J., Yang, J."Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial signaling pathway". Oncology Reports 28, no. 5 (2012): 1883-1888. https://doi.org/10.3892/or.2012.2000
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