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The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells

  • Authors:
    • Sanghun Lee
    • Min Cheol Kwon
    • Jun-Pil Jang
    • Jae Kyung Sohng
    • Hye Jin Jung
  • View Affiliations / Copyright

    Affiliations: Department of BT-Convergent Pharmaceutical Engineering, Sun Moon University, Tangjeong-myeon, Asan-si, Chungnam 336-708, Republic of Korea, Anticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, Chungbuk 363-883, Republic of Korea
    Copyright: © Lee et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 414-424
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    Published online on: June 23, 2017
       https://doi.org/10.3892/ijo.2017.4054
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Abstract

Glioblastoma (GBM) is the most aggressive and malignant form of primary brain cancer. Despite recent advances in cancer treatment, it remains a substantially incurable disease. Accordingly, more effective GBM therapeutic options are urgently required. In the present study, we investigated the anticancer effect of a ginsenoside metabolite, compound K (CK), against GBM cells. CK significantly inhibited not only growth, but also metastatic ability of U87MG and U373MG cells. CK arrested cell cycle progression at the G0/G1 phase with a decrease in the expression levels of cyclin D1 and cyclin D3 in both cell types. CK also induced apoptosis in GBM cells through nuclear condensation, an increase in ROS generation, mitochondrial membrane potential depolarization, and activation of caspase-3, caspase-9 and poly(ADP-ribose) polymerase (PARP). Furthermore, CK inhibited phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, contributing to the antiproliferative and apoptotic effects. Moreover, CK suppressed the self-renewal capacity as well as the invasiveness of U87MG and U373MG GBM stem-like cells (GSCs) by inducing a reduction in the expression of GSC markers, such as CD133, Nanog, Oct4 and Sox2. Taken together, our findings suggest that CK may potentially be useful for GBM treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Lee S, Kwon MC, Jang J, Sohng JK and Jung HJ: The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells. Int J Oncol 51: 414-424, 2017.
APA
Lee, S., Kwon, M.C., Jang, J., Sohng, J.K., & Jung, H.J. (2017). The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells. International Journal of Oncology, 51, 414-424. https://doi.org/10.3892/ijo.2017.4054
MLA
Lee, S., Kwon, M. C., Jang, J., Sohng, J. K., Jung, H. J."The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells". International Journal of Oncology 51.2 (2017): 414-424.
Chicago
Lee, S., Kwon, M. C., Jang, J., Sohng, J. K., Jung, H. J."The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells". International Journal of Oncology 51, no. 2 (2017): 414-424. https://doi.org/10.3892/ijo.2017.4054
Copy and paste a formatted citation
x
Spandidos Publications style
Lee S, Kwon MC, Jang J, Sohng JK and Jung HJ: The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells. Int J Oncol 51: 414-424, 2017.
APA
Lee, S., Kwon, M.C., Jang, J., Sohng, J.K., & Jung, H.J. (2017). The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells. International Journal of Oncology, 51, 414-424. https://doi.org/10.3892/ijo.2017.4054
MLA
Lee, S., Kwon, M. C., Jang, J., Sohng, J. K., Jung, H. J."The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells". International Journal of Oncology 51.2 (2017): 414-424.
Chicago
Lee, S., Kwon, M. C., Jang, J., Sohng, J. K., Jung, H. J."The ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells". International Journal of Oncology 51, no. 2 (2017): 414-424. https://doi.org/10.3892/ijo.2017.4054
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