Effect of insulin-like growth factor-I receptor on radiosensitivity of HepG2 cells
10.3760/cma.j.issn.1007-8118.2019.11.014
- VernacularTitle: 抑制胰岛素样生长因子-Ⅰ受体表达对肝癌细胞HepG2放射敏感性的影响和机制
- Author:
Dayong CAO
1
;
Zhen YAN
1
;
Bingyi SUN
1
;
Guoying LIN
1
;
Ning ZHANG
2
Author Information
1. Department of General Surgery Ⅱ, First Hospital of Qiqihaer, Qiqihaer 161000, Heilongjiang Province, China
2. Department of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Beijing 100853, China
- Publication Type:Journal Article
- Keywords:
Carcinoma, hepatocellular;
Radiation tolerance;
Cell cycle;
Insulin-like growth factor-Ⅰ receptor;
Survivin
- From:
Chinese Journal of Hepatobiliary Surgery
2019;25(11):855-859
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effect of insulin-like growth factor-Ⅰ (IGF-Ⅰ) receptor on radiosensitivity of HepG2 cells and the underlying mechanism.
Methods:HepG2 cells were divided into the following groups: negative control group, siRNA group, irradiation group and combined group. HepG2 cells were transfected with IGF-Ⅰ receptor siRNA combined with irradiation therapy to investigate the effect on cell proliferation by methyl thiazolyl tetrazolium and cell cycle using flow cytometry. Expression of IGF-Ⅰ receptor, proliferating cell nuclear antigen (PCNA), cyclin-dependent kinases 1(CDK1) and Survivin were detected using Western blotting and Q-PCR.
Results:The expression of IGF-Ⅰ receptor in HepG2 cells was decreased significantly after siRNA transfection compared with the control group. After the combinational therapy, cell viability was decreased significantly according with control group [(1.02±0.08) vs. (1.08± 0.10) vs. (0.60±0.07)]; In addition, cell cycle was arrested in G2/M[(20.3±0.3)% vs. (22.6±0.4)% vs. (34.7±0.5)%] and CDK1 expression was reduced significantly. The relative expression of Survivin in siRNA group was lower than negative control group, the difference was statistically significant (P<0.05).
Conclusion:Inhibition of IGF-Ⅰ receptor can enhance the radiosensitivity of HepG2 cells through cell cycle arrest.
