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作 者:郭芝刚[1] 曾军[1] 张锦宏[2] 何玉文[2]
机构地区:[1]广州医学院基础学院,510120 [2]广州医学院第一附属医院药剂科,510120
出 处:《重庆医学》2013年第8期850-852,共3页Chongqing medicine
基 金:广东省药学会基金资助项目(2011A12);广州市教育局课题资助项目(10A274);广州医学院基金资助项目(110508);广州医学院青年基金资助项目(098603)
摘 要:目的研究丁酸钠(NaB)抑制鼻咽癌细胞CNE2吲哚胺-吡咯2,3-双加氧酶(IDO)表达从而解除肿瘤免疫耐受的分子机制。方法体外培养人鼻咽癌上皮细胞CNE2,采用NaB和(或)IFN-γ处理CNE2细胞;免疫印迹检测CNE2细胞IDO的表达情况;RT-PCR检测JAK/STAT的细胞因子信号抑制因子1(SOCS1)和SOCS3的转录水平;Real time PCR检测CNE2细胞干扰素调节因子-1(IRF-1)的转录情况。结果在NaB作用下,CNE2细胞内IDO的表达减少,并且IFN-γ诱导的IDO表达也被显著抑制;SOCS1和SOCS3的转录水平未见改变;而IFN-γ诱导的IRF1转录受到NaB的显著抑制。结论 NaB抑制IFN-γ诱导的IDO表达,不是通过增加SOCS1和SOCS3的转录,而可能是通过下调IRF-1,抑制IFN-γ诱导的IDO表达。Objective To study the molecular mechanism of sodium butyrate(NaB) inhibiting CNE2 indoleamine-2,3-dioxygen- ase(IDO) expression in nasopharyngeal carcinoma cell line for unlocking cancer ceil immune tolerance. Methods Human nasopba- ryngeal carcinoma epithelial cells CNE2 were cultured in vitro and treated with NaB in the presence or absence of IFN-r. IDO ex- pression,JAK/STAT-SOCS1 and SOCS3 transcription of interferon regulatory factor-1 (IRF-1) in CNE2 cells were detected by Western blot,RT-PCR and real-time PCR,respectively. Results NaB and/or IFN-rinhibited IDO expression induced by IFN-7 in CNE2 cells,while transcription of SOCS1 and SOCS3 remained stable. Moreover, NaB significantly inhibited IFN-r-induced IRF-1 transcription. Conclusion NaB inhibiting IFN-r-induced IDO expression is not by increasing SOCS1 and SOCS3 transcription, but through down-regulation of IRF-1 transcription.
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