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Article

Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells

  • Authors:
    • Eun Jeong Choi
    • Jae-In Lee
    • Gun-Hee Kim
  • View Affiliations / Copyright

    Affiliations: Plant Resources Research Institute, Duksung Women's University, Tobong-ku, Seoul 132-714, Republic of Korea
  • Pages: 726-730
    |
    Published online on: January 8, 2013
       https://doi.org/10.3892/ijmm.2013.1230
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Abstract

In the present study, in order to investigate the anticancer effects of O-desmethylangolensin (O-DMA) on human hepatocellular carcinoma Hep3B cells, we first examined the antiproliferative effect of O-DMA. When Hep3B cells were treated with O-DMA at various concentrations (5-200 µM) for 24, 48 or 72 h, cell proliferation decreased significantly in a dose- and time-dependent manner. Moreover, O-DMA exposure at the IC50 concentration for 72 h arrested cells at the G2/M phase, which was accompanied by a reduction in CDK1, and an increase in cyclin A and B. Under the same conditions, O-DMA significantly increased the number of sub-G1 phase cells. Additionally, an Annexin V assay revealed that exposure to O-DMA affected the rate of cell apoptosis. O-DMA caused the downregulation of Bcl-2 and upregulation of Bax, which led to cytochrome c release from the mitochondria and activation of caspase-3. Taken together, these data suggest that O-DMA exhibits anticancer activity by arresting the cell cycle at G2/M phase and causing mitochondrial-dependent apoptosis in Hep3B cells.
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Copy and paste a formatted citation
Spandidos Publications style
Choi EJ, Lee J and Kim G: Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells. Int J Mol Med 31: 726-730, 2013.
APA
Choi, E.J., Lee, J., & Kim, G. (2013). Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells. International Journal of Molecular Medicine, 31, 726-730. https://doi.org/10.3892/ijmm.2013.1230
MLA
Choi, E. J., Lee, J., Kim, G."Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells". International Journal of Molecular Medicine 31.3 (2013): 726-730.
Chicago
Choi, E. J., Lee, J., Kim, G."Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells". International Journal of Molecular Medicine 31, no. 3 (2013): 726-730. https://doi.org/10.3892/ijmm.2013.1230
Copy and paste a formatted citation
x
Spandidos Publications style
Choi EJ, Lee J and Kim G: Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells. Int J Mol Med 31: 726-730, 2013.
APA
Choi, E.J., Lee, J., & Kim, G. (2013). Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells. International Journal of Molecular Medicine, 31, 726-730. https://doi.org/10.3892/ijmm.2013.1230
MLA
Choi, E. J., Lee, J., Kim, G."Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells". International Journal of Molecular Medicine 31.3 (2013): 726-730.
Chicago
Choi, E. J., Lee, J., Kim, G."Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells". International Journal of Molecular Medicine 31, no. 3 (2013): 726-730. https://doi.org/10.3892/ijmm.2013.1230
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