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Journal of Experimental & Clinical Cancer Research
Published in: Journal of Experimental & Clinical Cancer Research 1/2011

Open Access 01-12-2011 | Research

CpG oligonucleotides suppress HepG2 cells-induced Jurkat cell apoptosis via the Fas-FasL-mediated pathway

Authors: Jianfeng Zheng, Rongquan Fu, Jing Li, Xiaozhong Wang

Published in: Journal of Experimental & Clinical Cancer Research | Issue 1/2011

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Abstract

Objective

To explore the potential role of CpG motif-containing oligonucleotides (CpG-ODN) in modulating the expression of FasL in HepG2 and Fas in Jurkat cells in vitro, and to examine the effect of CpG-ODN treatment on the HepG2 cells-mediated Jurkat cell apoptosis in vitro.

Methods

The expressions of FasL in HepG2 and Fas in Jurkat cells were examined by real time PCR and flow cytometry (FCM). HepG2 and Jurkat cells were co-cultured, and the frequency of apoptotic Jurkat cells and levels of activated caspase-3 were determined by FCM.

Results

Treatment with CpG-ODN down-regulated the expression of FasL in HepG2 cells in a dose- and time-dependent manner. In addition, treatment with CpG-ODN down-regulated the Fas mRNA transcription and protein expression in Jurkat cells. Treatment of HepG2 cells or Jurkat cells with FasL-neutralizing antibody NOK-2 remarkably inhibited the HepG2-medaited Jurkat cell apoptosis. Pre-treatment of HepG2 or Jurkat cells with CpG-ODN significantly reduced the frequency of HepG2-mediated apoptotic Jurkat cells and inhibited the activation of caspase-3 in Jurkat cells in vitro.

Conclusions

Our data indicated that treatment with CpG-ODN inhibited the HepG2 cells-mediated Jurkat cell apoptosis by modulating the Fas/FasL pathway. Apparently, CpG-ODN treatment may be a potential therapeutic reagent for HCC.
Appendix
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Metadata
Title
CpG oligonucleotides suppress HepG2 cells-induced Jurkat cell apoptosis via the Fas-FasL-mediated pathway
Authors
Jianfeng Zheng
Rongquan Fu
Jing Li
Xiaozhong Wang
Publication date
01-12-2011
Publisher
BioMed Central
Published in
Journal of Experimental & Clinical Cancer Research / Issue 1/2011
Electronic ISSN: 1756-9966
DOI
https://doi.org/10.1186/1756-9966-30-48

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