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

<p>Abstract</p> <p>Objective</p> <p>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 <it>in vitro</it>, and to examine the effect of CpG-ODN treatment on th...

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Bibliographic Details
Main Authors: Li Jing, Fu Rongquan, Zheng Jianfeng, Wang Xiaozhong
Format: Article
Language:English
Published: BMC 2011-05-01
Series:Journal of Experimental & Clinical Cancer Research
Subjects:
Online Access:http://www.jeccr.com/content/30/1/48
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Summary:<p>Abstract</p> <p>Objective</p> <p>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 <it>in vitro</it>, and to examine the effect of CpG-ODN treatment on the HepG2 cells-mediated Jurkat cell apoptosis <it>in vitro</it>.</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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 <it>in vitro</it>.</p> <p>Conclusions</p> <p>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.</p>
ISSN:1756-9966