Sémat A, Duprey P, Vasseur M, Darmon M
Differentiation. 1986;31(1):61-6. doi: 10.1111/j.1432-0436.1986.tb00384.x.
When mouse-teratocarcinoma-derived fibroblasts (1246 cell line) are subjected to treatment with the inhibitor of DNA methylation, 5-Azacytidine (5 AzaC), they transiently express at 55-kilodalton intermediate-filament protein recognized by the epithelial-specific monoclonal antibody, TROMA-1, although they retain a fibroblastic morphology. However, rare clones (e.g., the 1339 cell line) that permanently express the antigen recognized by TROMA-1 can be derived from the 5 AzaC-treated 1246 population, and these clones have an epithelial phenotype. In the present study, we used cloned DNA probes to demonstrate that, in 1246 fibroblasts, 5 AzaC induces the appearance of Endo-A mRNA. High levels of Endo-A mRNA were also detected in the epithelial derivative, cell line 1339. In both cases, the capping site of the Endo-A mRNA was found to be the same as that in epithelial cells which normally express this RNA.
当源自小鼠畸胎癌的成纤维细胞(1246细胞系)用DNA甲基化抑制剂5-氮杂胞苷(5 AzaC)处理时,它们会短暂表达一种55千道尔顿的中间丝蛋白,该蛋白可被上皮特异性单克隆抗体TROMA-1识别,尽管它们仍保留成纤维细胞形态。然而,从经5 AzaC处理的1246细胞群体中可获得罕见的能永久表达被TROMA-1识别的抗原的克隆(例如1339细胞系),并且这些克隆具有上皮表型。在本研究中,我们使用克隆的DNA探针来证明,在1246成纤维细胞中,5 AzaC诱导Endo-A mRNA的出现。在上皮衍生物细胞系1339中也检测到了高水平的Endo-A mRNA。在这两种情况下,Endo-A mRNA的帽位点与正常表达该RNA的上皮细胞中的帽位点相同。