Effect of ginsenoside metabolite compound K on migration and invasion of human hepatocellular carcinoma line HepG2
10.3969/j.issn.1001-1978.2018.01.008
- VernacularTitle:人参皂苷CK对人肝癌细胞HepG2迁移及侵袭的影响
- Author:
ting Wen PENG
1
;
yi Wu SUN
;
chang Jia SUN
;
jia Jia DU
;
Wei WEI
Author Information
1. 安徽医科大学临床药理研究所
- Keywords:
ginsenoside CK;
HepG2 cell;
cell viabili-ty;
migration;
invasion;
epithelial mesenchymal transi-tion
- From:
Chinese Pharmacological Bulletin
2018;34(1):27-32
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of ginsen-oside metabolite compound K ( CK) on migration and invasion of human hepatocellular carcinoma line HepG2, and the possible signaling pathway underlying these processes .Methods HepG2 cells were exposed to ginsenoside CK (0, 10, 20, 40, 80 μmol· L-1 ) for 24 h.The cell viability was examined by MTT as-say, and the ability of migration and invasion was ob-served with the wound healing and transwell assay .The expression of E-cadherin , N-cadherin and other related signal molecules such as p-ERK, ERK, p-Akt, Akt were detected by Western blot .Results The cell via-bility was significantly reduced by ginsenoside CK (20, 40, 80 μmol· L-1) (P<0.01).The ability of cell migration and invasion was significantly inhibited after exposure to ginsenoside CK .After treatment with ginsenoside CK (20, 40, 80 μmol · L-1 ) in HepG2 cells, the expression of E-cadherin markedly in-creased, while N-cadherin expression significantly de-creased.Meanwhile, the expression of p-ERK and p-Akt decreased after treated with ginsenoside CK .Con-clusion Ginsenoside CK inhibits the migration and invasion of human hepatocellular carcinoma line HepG2, which may be through suppression of ERK and Akt signaling .
