Mechanism study on apoptosis of hepatocellular carcinoma HepG2 cells induced by ursolic acid through inhibiting the expression of miR-21
10.11665/j.issn.1000-5048.20150619
- VernacularTitle:乌索酸通过抑制miR-21表达诱导肝癌HepG2细胞凋亡的机制
- Author:
Kunmei LIU
1
;
Le GUO
;
Tao XI
Author Information
1. 宁夏医科大学颅脑疾病重点实验室；中国药科大学生命科学与技术学院
- Publication Type:Journal Article
- Keywords:
ursolic acid;
hepatocellular carcinoma cells;
miR-21;
proliferation;
apoptosis
- From:
Journal of China Pharmaceutical University
2015;46(6):745-750
- CountryChina
- Language:Chinese
-
Abstract:
This study aimed at investigating the effect of miR-21 on the apoptosis of hepatocellular carcinoma HepG2 cells induced by ursolic acid(UA). MTT assay was used to determine the inhibition effect of ursolic acid on proliferation of hepatocellular carcinoma cells. The expression level of miR-21 in hepatocellular carcinoma cells and the regulation effect of ursolic acid on the expression of miR-21 in HepG2 cells were determined by qPCR. To up-regulate the expression of miR-21, miR-21 mimics were transfected into HepG2 cells. Then MTT assay, flowcytometry(Annexin V-FITC staining), and RT-PCR were used to detect the regulation effects of ursolic acid on the proliferation, apoptosis, and the expression of apoptosis-related genes after miR-21 over-expression. The results showed that the proliferation inhibition effect of ursolic acid on HepG2 cells and the expression level of miR-21 in HepG2 cells were higher than in hepatic cell L-02 and hepatocellular carcinoma SMCC-7721, Bel-7402 cells. So further study was performed in the HepG2 cells. Ursolic acid inhibited the expression of miR-21 in HepG2 cells. And the greatest inhibition effect was at 24 h after treatment with UA. Over-expression of miR-21 partially offset the effects of ursolic acid on the proliferation, apoptosis, and the expression of apoptosis-related genes such as Bcl-2, survivin and Bax after 24 h. The results suggested that apoptosis of hepatocellular carcinoma HepG2 cells could be induced by ursolic acid by down-regulating the expression of miR-21.
