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Article Open Access

Solamargine triggers hepatoma cell death through apoptosis

  • Authors:
    • Xiaodong Xie
    • Haitao Zhu
    • Huijian Yang
    • Wensi Huang
    • Yingying Wu
    • Ying Wang
    • Yanling Luo
    • Dongqing Wang
    • Genbao Shao
  • View Affiliations / Copyright

    Affiliations: Department of Radiology, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China, Department of Immunology, Center of Clinical Medicine and Laboratory, Jiangsu University, Zhenjiang, Jiangsu 212013, P.R. China, Department of Biology, School of Medical Science and Laboratory Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, P.R. China
    Copyright: © Xie et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 168-174
    |
    Published online on: May 11, 2015
       https://doi.org/10.3892/ol.2015.3194
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Abstract

Solamargine (SM), a steroidal alkaloid glycoside extracted from the traditional Chinese herb Solanum incanum, has been evidenced to inhibit the growth and induce apoptosis in a number of human cancer cell lines. In the present study, the anticancer effect of SM and underlying molecular mechanism of SM‑induced apoptosis were investigated on the human hepatocellular carcinoma cells, SMMC7721 and HepG2. The proliferation effects of SM on the SMMC7721 and HepG2 cell lines were evaluated using MTT and colony formation assays. In addition, the percentage of apoptosis was measured using an Annexin V/propidium iodide staining method and the cell cycle distribution mediated by SM was analyzed using flow cytometry. The expression levels of B‑cell lymphoma‑2 (Bcl‑2), Bcl‑2‑associated X protein (Bax), caspase‑3, caspase‑9, proliferating cell nuclear antigen (pcna) and Ki67 proteins were examined to further demonstrate the proliferate and apoptosis effects of SM on the hepatoma cells. The results indicated that SM effectively inhibited hepatoma cell proliferation and promoted apoptosis. SM resulted in cell cycle arrest at the G2/M phase in the two cell lines. In addition, SM downregulated the levels of proliferation‑associated (Ki67 and pcna) and anti‑apoptotic (Bcl‑2) proteins, and promoted the activity of apoptosis‑associated proteins (Bax, caspase‑3 and caspase‑9). Therefore, the activation of the Bcl‑2/Bax and caspase signaling pathways may be involved in the SM-induced apoptosis of hepatoma cells.
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Copy and paste a formatted citation
Spandidos Publications style
Xie X, Zhu H, Yang H, Huang W, Wu Y, Wang Y, Luo Y, Wang D and Shao G: Solamargine triggers hepatoma cell death through apoptosis. Oncol Lett 10: 168-174, 2015.
APA
Xie, X., Zhu, H., Yang, H., Huang, W., Wu, Y., Wang, Y. ... Shao, G. (2015). Solamargine triggers hepatoma cell death through apoptosis. Oncology Letters, 10, 168-174. https://doi.org/10.3892/ol.2015.3194
MLA
Xie, X., Zhu, H., Yang, H., Huang, W., Wu, Y., Wang, Y., Luo, Y., Wang, D., Shao, G."Solamargine triggers hepatoma cell death through apoptosis". Oncology Letters 10.1 (2015): 168-174.
Chicago
Xie, X., Zhu, H., Yang, H., Huang, W., Wu, Y., Wang, Y., Luo, Y., Wang, D., Shao, G."Solamargine triggers hepatoma cell death through apoptosis". Oncology Letters 10, no. 1 (2015): 168-174. https://doi.org/10.3892/ol.2015.3194
Copy and paste a formatted citation
x
Spandidos Publications style
Xie X, Zhu H, Yang H, Huang W, Wu Y, Wang Y, Luo Y, Wang D and Shao G: Solamargine triggers hepatoma cell death through apoptosis. Oncol Lett 10: 168-174, 2015.
APA
Xie, X., Zhu, H., Yang, H., Huang, W., Wu, Y., Wang, Y. ... Shao, G. (2015). Solamargine triggers hepatoma cell death through apoptosis. Oncology Letters, 10, 168-174. https://doi.org/10.3892/ol.2015.3194
MLA
Xie, X., Zhu, H., Yang, H., Huang, W., Wu, Y., Wang, Y., Luo, Y., Wang, D., Shao, G."Solamargine triggers hepatoma cell death through apoptosis". Oncology Letters 10.1 (2015): 168-174.
Chicago
Xie, X., Zhu, H., Yang, H., Huang, W., Wu, Y., Wang, Y., Luo, Y., Wang, D., Shao, G."Solamargine triggers hepatoma cell death through apoptosis". Oncology Letters 10, no. 1 (2015): 168-174. https://doi.org/10.3892/ol.2015.3194
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