Inhibitory effect of asiatic acid on human liver carcinoma cells via cell cycle blockage and apoptosis induction
10.3872/j.issn.1007-385x.2019.05.004
- VernacularTitle:积雪草酸通过细胞周期阻滞和诱导凋亡抑制人肝癌Huh7细胞
- Author:
GUO Bingjie
1
;
ZHAO Shasha
1
;
LING Changquan
1
Author Information
1. (Department of Traditional Chinese Medicine, Naval Military Medical University
- Publication Type:Journal Article
- Keywords:
asiatic acid(AA);
liver carcinoma;
Huh7 cell;
proliferation;
apoptosis;
MAPK;
PI3K/AKT
- From:
Chinese Journal of Cancer Biotherapy
2019;26(5):506-511
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the inhibitory effect of asiatic acid (AA) on malignant biological behaviors of human liver cancer cells and to explore the mechanism. Methods: Human liver cancer cell line (Huh7) was used as research subject, and treated with different concentrations of AA (0, 5, 10, 25, 50, 100 μmol/L) in vitro. The effect of AA on cell proliferation was determined by CCK-8 and EdU assay; the apoptosis and cell cycle distribution were detected by flow cytometry, while the expressions of apoptosis-related proteins (AKT, P-ERK 1/2 , p38, cleaved-caspase3, cleaved-caspase9, BAX, Bcl-2, AKT, ERK, p38, pro-caspase 3 and pro-caspase 9) were examined by WB. Results: AA could inhibit the proliferation of Huh7 cells in a dose- and time-dependent manner (all P<0.05). After being incubated with 10 μmol/L AA for 24 h, the proliferation of Huh7 cells was significantly inhibited (P<0.05), the apoptosis rate was significantly increased (P<0.05), and cell cycle was arrested in G1 phase (P<0.05).AAinduced p-p38 expression, but inhibited the expression of p-AKT and p-ERK in a dose-dependent manner (all P<0.05). In addition, as the concentration of AA increased, the levels of cleaved-caspase 3, cleaved-caspase 9 and BAX increased, while the level of Bcl-2 decreased (all P<0.05). Conclusion:AAinhibits the proliferation of human liver cancer cells and promotes its apoptosis, which is associated with the MAPK and PI3K/AKT pathways.
- Full text:20190504.pdf
