Compound K attenuates stromal cell-derived growth factor 1 (SDF-1)-induced migration of C6 glioma cells.
10.4162/nrp.2016.10.3.259
- Author:
Hyuck KIM
1
;
Hyo Sun ROH
;
Jai Eun KIM
;
Sun Dong PARK
;
Won Hwan PARK
;
Jin Young MOON
Author Information
1. Department of Diagnostics, College of Korean Medicine, Dongguk University, Goyang 10326, Korea.
- Publication Type:Original Article
- Keywords:
Panax ginseng;
compound K;
SDF-1;
anti-tumor;
C6 glioma
- MeSH:
Blotting, Western;
Cell Movement;
Cell Survival;
Gastrointestinal Microbiome;
Glioma*;
Matrix Metalloproteinases;
Metalloproteases;
Panax;
Phosphorylation;
Phosphotransferases;
Protein Kinase C;
Wound Healing
- From:Nutrition Research and Practice
2016;10(3):259-264
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/OBJECTIVES: Stromal cell-derived growth factor 1 (SDF-1), also known as chemokine ligand 12, and chemokine receptor type 4 are involved in cancer cell migration. Compound K (CK), a metabolite of protopanaxadiol-type ginsenoside by gut microbiota, is reported to have therapeutic potential in cancer therapy. However, the inhibitory effect of CK on SDF-1 pathway-induced migration of glioma has not yet been established. MATERIALS/METHODS: Cytotoxicity of CK in C6 glioma cells was determined using an EZ-Cytox cell viability assay kit. Cell migration was tested using the wound healing and Boyden chamber assay. Phosphorylation levels of protein kinase C (PKC)α and extracellular signal-regulated kinase (ERK) were measured by western blot assay, and matrix metallopeptidases (MMP) were measured by gelatin-zymography analysis. RESULTS: CK significantly reduced the phosphorylation of PKCα and ERK1/2, expression of MMP9 and MMP2, and inhibited the migration of C6 glioma cells under SDF-1-stimulated conditions. CONCLUSIONS: CK is a cell migration inhibitor that inhibits C6 glioma cell migration by regulating its downstream signaling molecules including PKCα, ERK1/2, and MMPs.
