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Article

Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways

  • Authors:
    • Xianqing Guo
    • Xiao Ding
  • View Affiliations / Copyright

    Affiliations: Department of Pharmaceuticals, Qilu Hospital of Shandong University, Qingdao, Shandong 266035, P.R. China, Department of Gynecology and Obstetrics, Qilu Hospital of Shandong University, Qingdao, Shandong 266035, P.R. China
  • Pages: 9537-9542
    |
    Published online on: April 10, 2018
       https://doi.org/10.3892/ol.2018.8454
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Abstract

Diosgenin is a natural steroidal saponin that is extracted from a range of sources, including from fenugreek. It is a critical raw material in the synthesis of steroid hormone drugs, exhibiting antitumor, anti‑inflammatory, antioxidation and a number of other significant pharmacological actions, possessing high pharmaceutical value. The aim of the present study was to investigate the effects of dioscin suppression on ovarian cancer cell growth and the mechanism of apoptosis induction by dioscin in ovarian cancer cells. The results of the present study demonstrated that dioscin decreased viability and induced apoptosis in SKOV3 human ovarian cancer cells in a dose‑dependent manner. Dioscin significantly increased caspase‑3 and caspase‑9 activity, and increased the protein expression of Bax and cleaved poly(ADP‑ribose) polymerase in SKOV3 cells. In addition, dioscin significantly suppressed vascular endothelial growth factor receptor (VEGFR)2, phosphoinositide 3‑kinase (PI3K), phosphorylated AKT and phosphorylated p38 mitogen‑activated protein kinase (MAPK) protein expression in SKOV3 cells. Taken together, to the best of our knowledge, the present study demonstrated for the first time that dioscin suppresses cell viability in ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways.
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Copy and paste a formatted citation
Spandidos Publications style
Guo X and Ding X: Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways. Oncol Lett 15: 9537-9542, 2018.
APA
Guo, X., & Ding, X. (2018). Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways. Oncology Letters, 15, 9537-9542. https://doi.org/10.3892/ol.2018.8454
MLA
Guo, X., Ding, X."Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways". Oncology Letters 15.6 (2018): 9537-9542.
Chicago
Guo, X., Ding, X."Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways". Oncology Letters 15, no. 6 (2018): 9537-9542. https://doi.org/10.3892/ol.2018.8454
Copy and paste a formatted citation
x
Spandidos Publications style
Guo X and Ding X: Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways. Oncol Lett 15: 9537-9542, 2018.
APA
Guo, X., & Ding, X. (2018). Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways. Oncology Letters, 15, 9537-9542. https://doi.org/10.3892/ol.2018.8454
MLA
Guo, X., Ding, X."Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways". Oncology Letters 15.6 (2018): 9537-9542.
Chicago
Guo, X., Ding, X."Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways". Oncology Letters 15, no. 6 (2018): 9537-9542. https://doi.org/10.3892/ol.2018.8454
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