Preliminary study on the mechanism of halofuginone inhibiting the activity of HepG2 cells
10.16438/j.0513-4870.2023-0216
- VernacularTitle:常山酮抑制肝癌HepG2细胞活性及机制初步研究
- Author:
Meng-yang CHEN
1
,
2
;
Rui-ping HUAI
1
,
2
;
Dan-ni YANG
1
,
2
;
Li-jie LEI
1
,
2
;
Qiu-lin PU
1
,
2
;
Li-li XIONG
3
Author Information
1. School of Life Science and Engineering, Southwest Jiaotong University, Chengdu 610000, China
2. School of Chemistry, Southwest Jiaotong University, Chengdu 610000, China
3. School of Chemistry, Southwest Jiaotong University, Chengdu 610000, China
- Publication Type:Research Article
- Keywords:
halofuginone;
tricarboxylic acid;
HepG2 cell;
isocitrate dehydrogenase;
aerobic metabolism
- From:
Acta Pharmaceutica Sinica
2024;59(2):368-373
- CountryChina
- Language:Chinese
-
Abstract:
This study aimed to investigate halofuginone's inhibitory effect and mechanism on the activity of hepatocellular carcinoma cells. HepG2 cells were used to detect the effects of halofuginone. After treatment, cell activity, cell migration, cell cycle, and cell apoptosis were detected by CCK-8, transwell, and flow cytometry, respectively. The expression levels of growth and metabolism-related factors such as citrate synthase (CS), ketoglutarate dehydrogenase (OGDH), and isocitrate deoxygenase (IDH) were detected by real-time quantitative PCR and Western blot. Compared with the control group, the activity of HepG2 cells was significantly inhibited by halofuginone (P < 0.01), the migration rate of HepG2 cells was decreased (P < 0.01), the apoptosis of HepG2 cells was induced (P < 0.01), and the cell cycle was arrested in S phase (P < 0.01). The expression levels of tricarboxylic acid key enzymes CS, IDH3, and OGDH were up-regulated, the expression level of isocitrate dehydrogenase isoenzymes IDH1 and IDH2 were down-regulation. In conclusion, halofuginone can inhibit the proliferation and migration of HepG2 cells and promote apoptosis in a dose-dependent manner, which may be due to the promotion of the aerobic metabolism of cells.
