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Title 

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

Authors 

S LeeMin Cheol KwonJun-Pil JangJ SohngH J Jung

Publisher 

Spandidos Publications

Issue Date 

2017

Citation 

International Journal of Oncology

Keywords 

Anticancer effectCompound KGinsenosideGlioblastomaGlioblastoma stem-like cells

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 significa ntly i nhibited 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.

ISSN 

1019-6439

Link 

http://dx.doi.org/10.3892/ijo.2017.4054

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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