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

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dc.contributor.authorS Lee-
dc.contributor.authorMin Cheol Kwon-
dc.contributor.authorJun-Pil Jang-
dc.contributor.authorJ Sohng-
dc.contributor.authorH J Jung-
dc.date.accessioned2017-08-29-
dc.date.available2017-08-29-
dc.date.issued2017-
dc.identifier.issn1019-6439-
dc.identifier.uri10.3892/ijo.2017.4054ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/17269-
dc.description.abstractGlioblastoma (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.-
dc.publisherSpandidos Publ Ltd-
dc.titleThe ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells-
dc.title.alternativeThe ginsenoside metabolite compound K inhibits growth, migration and stemness of glioblastoma cells-
dc.typeArticle-
dc.citation.titleInternational Journal of Oncology-
dc.citation.number2-
dc.citation.endPage424-
dc.citation.startPage414-
dc.citation.volume51-
dc.contributor.affiliatedAuthorMin Cheol Kwon-
dc.contributor.affiliatedAuthorJun-Pil Jang-
dc.contributor.alternativeName이상훈-
dc.contributor.alternativeName권민철-
dc.contributor.alternativeName장준필-
dc.contributor.alternativeName송재경-
dc.contributor.alternativeName정혜진-
dc.identifier.bibliographicCitationInternational Journal of Oncology, vol. 51, no. 2, pp. 414-424-
dc.identifier.doi10.3892/ijo.2017.4054-
dc.subject.keywordAnticancer effect-
dc.subject.keywordCompound K-
dc.subject.keywordGinsenoside-
dc.subject.keywordGlioblastoma-
dc.subject.keywordGlioblastoma stem-like cells-
dc.subject.localAnti-cancer effect-
dc.subject.localAnticancer effect-
dc.subject.localanti-cancer effect-
dc.subject.localAnti-cancer effects-
dc.subject.localCompound K-
dc.subject.localginsenoside-
dc.subject.localGinsenoside-
dc.subject.localGinsenosides-
dc.subject.localglioblastoma-
dc.subject.localGlioblastoma-
dc.subject.localGlioblastoma stem-like cells-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Chemical Biology Research Center > 1. Journal Articles
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