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Article

Effect of ximenynic acid on cell cycle arrest and apoptosis and COX-1 in HepG2 cells

  • Authors:
    • Fang Cai
    • Jianying Li
    • Yandi Liu
    • Zunyi Zhang
    • D. S. Hettiarachchi
    • Duo Li
  • View Affiliations / Copyright

    Affiliations: Department of Food Science and Nutrition, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China, Institute of Developmental and Regenerative Biology, Hangzhou Normal University, Hangzhou, Zhejiang 310000, P.R. China, School of Pharmacy, Curtin Health Innovation Research Institute, Curtin University, Perth 02042G, Australia
  • Pages: 5667-5676
    |
    Published online on: November 3, 2016
       https://doi.org/10.3892/mmr.2016.5920
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Abstract

Ximenynic acid is a conjugated enyne fatty acid, which is currently of interest due to its anti-inflammatory activity. Due to the association between inflammation and cancer, the present study was designed to investigate the anti‑cancer activity of ximenynic acid in the HepG2 human hepatoma cell line and the underlying mechanisms. The current study demonstrated the anti‑proliferation and pro‑apoptosis activities of ximenynic acid by cell viability assay and flow cytometry analysis. The expression of anti‑apoptosis protein silent information regulator T1 (SIRT1) was significantly suppressed by ximenynic acid. Furthermore, ximenynic acid blocked G1/S phase transition by inhibiting the protein expression of the cell cycle‑associated protein general control of amino acid synthesis yeast homolog like 2 (GCN5L2), and the mRNA expression of cyclin D3 and cyclin E1. Furthermore, ximenynic acid suppressed the expression of angiogenesis‑associated genes, including vascular endothelial growth factor (VEGF)‑B and VEGF‑C. Finally, ximenynic acid significantly inhibited the expression of cyclooxygenase‑1 (COX‑1) mRNA and protein, however COX‑2 expression was not reduced. The results of the present study suggested that ximenynic acid may inhibit growth of HepG2 cells by selective inhibition of COX‑1 expression, which leads to cell cycle arrest, and alters the apoptosis pathway and expression of angiogenic factors. The current study aimed to investigate whether ximenynic acid might be developed as novel anticancer agent.
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Copy and paste a formatted citation
Spandidos Publications style
Cai F, Li J, Liu Y, Zhang Z, Hettiarachchi DS and Li D: Effect of ximenynic acid on cell cycle arrest and apoptosis and COX-1 in HepG2 cells. Mol Med Rep 14: 5667-5676, 2016.
APA
Cai, F., Li, J., Liu, Y., Zhang, Z., Hettiarachchi, D.S., & Li, D. (2016). Effect of ximenynic acid on cell cycle arrest and apoptosis and COX-1 in HepG2 cells. Molecular Medicine Reports, 14, 5667-5676. https://doi.org/10.3892/mmr.2016.5920
MLA
Cai, F., Li, J., Liu, Y., Zhang, Z., Hettiarachchi, D. S., Li, D."Effect of ximenynic acid on cell cycle arrest and apoptosis and COX-1 in HepG2 cells". Molecular Medicine Reports 14.6 (2016): 5667-5676.
Chicago
Cai, F., Li, J., Liu, Y., Zhang, Z., Hettiarachchi, D. S., Li, D."Effect of ximenynic acid on cell cycle arrest and apoptosis and COX-1 in HepG2 cells". Molecular Medicine Reports 14, no. 6 (2016): 5667-5676. https://doi.org/10.3892/mmr.2016.5920
Copy and paste a formatted citation
x
Spandidos Publications style
Cai F, Li J, Liu Y, Zhang Z, Hettiarachchi DS and Li D: Effect of ximenynic acid on cell cycle arrest and apoptosis and COX-1 in HepG2 cells. Mol Med Rep 14: 5667-5676, 2016.
APA
Cai, F., Li, J., Liu, Y., Zhang, Z., Hettiarachchi, D.S., & Li, D. (2016). Effect of ximenynic acid on cell cycle arrest and apoptosis and COX-1 in HepG2 cells. Molecular Medicine Reports, 14, 5667-5676. https://doi.org/10.3892/mmr.2016.5920
MLA
Cai, F., Li, J., Liu, Y., Zhang, Z., Hettiarachchi, D. S., Li, D."Effect of ximenynic acid on cell cycle arrest and apoptosis and COX-1 in HepG2 cells". Molecular Medicine Reports 14.6 (2016): 5667-5676.
Chicago
Cai, F., Li, J., Liu, Y., Zhang, Z., Hettiarachchi, D. S., Li, D."Effect of ximenynic acid on cell cycle arrest and apoptosis and COX-1 in HepG2 cells". Molecular Medicine Reports 14, no. 6 (2016): 5667-5676. https://doi.org/10.3892/mmr.2016.5920
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