Role of ERK/FoxO3a signal axis in inhibitory effect of vitexin 1 (VB-1) in HepG2 cell proliferation.
- Author:
Xing-Xing ZHENG
;
Ren-Shuo ZHANG
;
Ying-Jun ZHOU
;
Jian-Gang WANG
- Publication Type:Journal Article
- MeSH: Apigenin; pharmacology; Carcinoma, Hepatocellular; drug therapy; genetics; metabolism; physiopathology; Cell Proliferation; drug effects; Drugs, Chinese Herbal; pharmacology; Extracellular Signal-Regulated MAP Kinases; genetics; metabolism; Forkhead Box Protein O3; Forkhead Transcription Factors; genetics; metabolism; Growth Inhibitors; pharmacology; Hep G2 Cells; Humans; Liver Neoplasms; drug therapy; genetics; metabolism; physiopathology; Signal Transduction; drug effects
- From: China Journal of Chinese Materia Medica 2014;39(7):1276-1279
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether the ERK/FoxO3a signal axis could induce the inhibitory effect of vitexin 1 (VB-1) in HepG2 cell proliferation.
METHODThe MTT method was adopted to observe the effect of different concentrations of VB-1 on human hepatoma carcinoma cell line HepG2 and immortalized human embryo liver cell line L-02. The cell growth was assessed by the clone formation assay. The protein phosphorylation levels of ERK1/2 and FoxO3a were measured by the western blot.
RESULTVB-1 inhibited the viability of HepG2 cell line in a concentration-dependent manner, with a weak effect on L-02 cell line. VB-1 could effectively inhibit the anchorage-dependent growth of HepG2 cells, and reduce the expression levels of pERK1/2 and pFoxO3a in a concentration-dependent manner. MEK1/2 inhibitor PD98059 could enhance VB-1' s effect in inhibiting HepG2 cell proliferation and ERK1/2, FoxO3a phosphorylation.
CONCLUSIONVB-1 inhibits the proliferative activity of hepatoma carcinoma cell line HepG2 by blocking the ERK/FoxO3a signal axis.