PMID- 28656196
OWN - NLM
STAT- MEDLINE
DCOM- 20180525
LR  - 20190115
IS  - 1791-2423 (Electronic)
IS  - 1019-6439 (Print)
IS  - 1019-6439 (Linking)
VI  - 51
IP  - 2
DP  - 2017 Aug
TI  - The ginsenoside metabolite compound K inhibits growth, migration and stemness of 
      glioblastoma cells.
PG  - 414-424
LID - 10.3892/ijo.2017.4054 [doi]
AB  - 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.
FAU - Lee, Sanghun
AU  - Lee S
AD  - Department of BT-Convergent Pharmaceutical Engineering, Sun Moon University, 
      Tangjeong-myeon, Asan-si, Chungnam 336-708, Republic of Korea.
FAU - Kwon, Min Cheol
AU  - Kwon MC
AD  - Anticancer Agent Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Cheongju, Chungbuk 363-883, Republic of Korea.
FAU - Jang, Jun-Pil
AU  - Jang JP
AD  - Anticancer Agent Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Cheongju, Chungbuk 363-883, Republic of Korea.
FAU - Sohng, Jae Kyung
AU  - Sohng JK
AD  - Department of BT-Convergent Pharmaceutical Engineering, Sun Moon University, 
      Tangjeong-myeon, Asan-si, Chungnam 336-708, Republic of Korea.
FAU - Jung, Hye Jin
AU  - Jung HJ
AD  - Department of BT-Convergent Pharmaceutical Engineering, Sun Moon University, 
      Tangjeong-myeon, Asan-si, Chungnam 336-708, Republic of Korea.
LA  - eng
PT  - Journal Article
DEP - 20170623
PL  - Greece
TA  - Int J Oncol
JT  - International journal of oncology
JID - 9306042
RN  - 0 (Ginsenosides)
RN  - 0 (Neoplasm Proteins)
RN  - A9RLM212CY (ginsenoside M1)
SB  - IM
MH  - Apoptosis/drug effects
MH  - Cell Line, Tumor
MH  - Cell Movement/drug effects
MH  - Cell Proliferation/drug effects
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Ginsenosides/*administration & dosage/chemistry
MH  - Glioblastoma/*drug therapy/genetics/pathology
MH  - Humans
MH  - Neoplasm Proteins/*genetics
MH  - Neoplastic Stem Cells/drug effects
MH  - Signal Transduction/drug effects
PMC - PMC5505016
EDAT- 2017/06/29 06:00
MHDA- 2018/05/26 06:00
PMCR- 2017/06/23
CRDT- 2017/06/29 06:00
PHST- 2017/04/14 00:00 [received]
PHST- 2017/06/14 00:00 [accepted]
PHST- 2017/06/29 06:00 [pubmed]
PHST- 2018/05/26 06:00 [medline]
PHST- 2017/06/29 06:00 [entrez]
PHST- 2017/06/23 00:00 [pmc-release]
AID - ijo-51-02-0414 [pii]
AID - 10.3892/ijo.2017.4054 [doi]
PST - ppublish
SO  - Int J Oncol. 2017 Aug;51(2):414-424. doi: 10.3892/ijo.2017.4054. Epub 2017 Jun 
      23.