Effects of Poly I:C in inducing growth inhibition and apoptosis of human hepatocellular carcinoma cells.
- Author:
Peng SHEN
1
;
Ting-Wan JIANG
;
Hui-Qi LU
;
Ling-Zhen ZHANG
;
Huan-Xing HAN
;
Rong-Cheng LUO
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Carcinoma, Hepatocellular; pathology; Cell Line, Tumor; Cell Proliferation; drug effects; Dose-Response Relationship, Drug; Humans; Interferon-beta; genetics; metabolism; Liver Neoplasms; pathology; Poly I-C; pharmacology; RNA, Messenger; genetics; metabolism; Receptors, Cholecystokinin; metabolism; Signal Transduction; Toll-Like Receptor 3; genetics; metabolism
- From: Journal of Southern Medical University 2009;29(3):525-527
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect and mechanism of Poly I:C in inducing growth inhibition and apoptosis of human hepatocellular carcinoma SMMC-7721 cells.
METHODSSMMC-7721 cells were treated with different doses of Poly I:C for 24, 48, and 72 h, and the cell growth inhibition rate was analyzed with CCK-8 assay. The cell cycle and the apoptosis were analyzed using flow cytometry with Annexin-V and PI staining, and quantitative RT-PCR analysis were used to detect the expression of TLR3, TRIF, and IFN-beta mRNA in cells.
RESULTSIn the cells exposed to Poly I:C at low, moderate, and high doses, the inhibitory rates was the highest in high-dose Poly I:C group, and at a given Poly I:C dose, prolonged exposure resulted in significantly increased cell growth inhibition rate (P<0.05). Flow cytometry showed that Poly I:C induced cell apoptosis in a time- and dose-dependent manner and significantly increased the percentage of G1-phase cells as compared with that in the control group. The mRNA level of TLR3, TRIF, and IFN-beta were also increased following Poly I:C treatment in comparison with the control group.
CONCLUSIONPoly I:C can induce significant growth inhibition and apoptosis of SMMC-7721 cells in a dose- and time-dependent manner possibly by causing cell cycle arrest and TLR3 signaling pathway activation that leads to IFN-beta production and cell apoptosis.