[Effects of Poly I:C in inducing growth inhibition and apoptosis of human hepatocellular carcinoma cells]

Nan Fang Yi Ke Da Xue Xue Bao. 2009 Mar;29(3):525-7.
[Article in Chinese]

Abstract

Objective: To explore the effect and mechanism of Poly I:C in inducing growth inhibition and apoptosis of human hepatocellular carcinoma SMMC-7721 cells.

Methods: SMMC-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.

Results: In 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.

Conclusion: Poly 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.

MeSH terms

  • Apoptosis / drug effects*
  • Carcinoma, Hepatocellular / pathology*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Dose-Response Relationship, Drug
  • Humans
  • Interferon-beta / genetics
  • Interferon-beta / metabolism
  • Liver Neoplasms / pathology*
  • Poly I-C / pharmacology*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Receptors, Cholecystokinin / metabolism
  • Signal Transduction
  • Toll-Like Receptor 3 / genetics
  • Toll-Like Receptor 3 / metabolism

Substances

  • RNA, Messenger
  • Receptors, Cholecystokinin
  • TLR3 protein, human
  • Toll-Like Receptor 3
  • Interferon-beta
  • Poly I-C