Croce Michela, De Ambrosis Alessandro, Corrias Maria V, Pistoia Vito, Occhino Marzia, Meazza Raffaella, Giron-Michel Julien, Azzarone Bruno, Accolla Roberto S, Ferrini Silvano
Istituto Nazionale per la Ricerca sul Cancro, 16132 Genoa, Italy.
Oncogene. 2003 Oct 30;22(49):7848-57. doi: 10.1038/sj.onc.1207054.
The HLA class II expression is controlled by the transcriptional activator CIITA. The transcription of CIITA is controlled by different promoters, among which promoter-IV is inducible by IFN-gamma. We analysed the regulation of HLA class II molecules by IFN-gamma in a large series of human neuroblastoma cell lines. No induction of surface or intracellular HLA class II molecules and of specific mRNA was observed, in all neuroblastomas, with the exception of a nonprototypic cell line, ACN. In a large subset of neuroblastomas IFN-gamma induced expression of CIITA mRNA, derived from promoter-IV, which was not methylated. In contrast, in another subset of neuroblastomas, CIITA was not inducible by IFN-gamma and CIITA promoter-IV was either completely or partially methylated. Interestingly, the use of DNA demethylating agents restored CIITA gene transcriptional activation by IFN-gamma, but not HLA class II expression. The defect of HLA class II was not related to alterations in RFX or NF-Y transcription factors, as suggested by EMSA or RFX gene transfection experiments. In addition, the transfection of a functional CIITA cDNA failed to induce HLA class II expression in typical neuroblastoma cells. Confocal microscopy and Western blot analysis suggested a defective nuclear translocation and/or reduced protein synthesis in CIITA-transfected NB cells. Altogether, these data point to multiple mechanisms preventing HLA class II expression in the neuroblastoma, either involving CIITA promoter-IV silencing, or acting at the CIITA post-transcriptional level.
HLA - II类分子的表达受转录激活因子CIITA调控。CIITA的转录由不同启动子控制,其中启动子IV可被IFN -γ诱导。我们在一系列人神经母细胞瘤细胞系中分析了IFN -γ对HLA - II类分子的调控。除了一个非典型细胞系ACN外,在所有神经母细胞瘤中均未观察到表面或细胞内HLA - II类分子及特异性mRNA的诱导表达。在大部分神经母细胞瘤中,IFN -γ诱导了源自未甲基化的启动子IV的CIITA mRNA的表达。相反,在另一部分神经母细胞瘤中,CIITA不能被IFN -γ诱导,且CIITA启动子IV完全或部分甲基化。有趣的是,使用DNA去甲基化剂可恢复IFN -γ对CIITA基因的转录激活,但不能恢复HLA - II类分子的表达。如EMSA或RFX基因转染实验所示,HLA - II类分子的缺陷与RFX或NF - Y转录因子的改变无关。此外,转染功能性CIITA cDNA未能在典型神经母细胞瘤细胞中诱导HLA - II类分子的表达。共聚焦显微镜和蛋白质印迹分析表明,在CIITA转染的神经母细胞瘤细胞中存在核转位缺陷和/或蛋白质合成减少。总之,这些数据表明存在多种机制阻止神经母细胞瘤中HLA - II类分子的表达,要么涉及CIITA启动子IV沉默,要么作用于CIITA转录后水平。