Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: CpG oligonucleotides suppress HepG2 cells-induced Jurkat cell apoptosis via the Fas-FasL-mediated pathway | Zheng et al. Journal of Experimental Clinical Cancer Research 2011 30 48 http content 30 1 48 RESEARCH Journal of Experimental Clinical Cancer Research Open Access CpG oligonucleotides suppress HepG2 cells-induced Jurkat cell apoptosis via the Fas-FasL-mediated pathway Jianfeng Zheng1t Rongquan Fu2t Jing Li3 and Xiaozhong Wang1 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 timedependent 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. Keywords CpG-ODN hepatocellular carcinoma apoptosis Introduction Tumors escape immune surveillance through multiple mechanisms. For example tumors can produce inhibitory factors such as transforming growth factor-b TGF-b and vascular endothelial growth factor VEGF leading to the reduced dendritic cell
