Banerjee R, Karpen S, Siekevitz M, Lengyel G, Bauer J, Acs G
Department of Neoplastic Diseases, Mount Sinai School of Medicine, City University of New York, New York 10029.
Hepatology. 1989 Dec;10(6):1008-13. doi: 10.1002/hep.1840100620.
Tumor necrosis factor-alpha is an inducer of acute-phase protein synthesis in liver cells. The mechanism by which tumor necrosis factor-alpha alters gene expression in these cells is largely unknown. In this study, we demonstrate that tumor necrosis factor-alpha stimulates human immunodeficiency virus-1 long terminal repeat-promoted gene expression in the human hepatoblastoma HepG2 cell line and increased binding of trans-activating factors to kappa B (kappa B) DNA sequences. In contrast to lymphocytic cells where the nuclear factors recognizing the kappa B sequences are activated by both tumor necrosis factor-alpha and phorbol-12-myristate-13-acetate through a posttranslational mechanism, in HepG2 cells phorbol-12-myristate-13-acetate does not activate these factor(s), and de novo protein synthesis seems to be required in HepG2 cells for gene activation by tumor necrosis factor-alpha.
肿瘤坏死因子-α是肝细胞中急性期蛋白合成的诱导剂。肿瘤坏死因子-α改变这些细胞中基因表达的机制在很大程度上尚不清楚。在本研究中,我们证明肿瘤坏死因子-α刺激人免疫缺陷病毒1型长末端重复序列促进的基因在人肝癌细胞系HepG2中的表达,并增加反式激活因子与κB(kappa B)DNA序列的结合。与淋巴细胞不同,在淋巴细胞中识别κB序列的核因子可通过翻译后机制被肿瘤坏死因子-α和佛波醇-12-肉豆蔻酸酯-13-乙酸酯激活,而在HepG2细胞中,佛波醇-12-肉豆蔻酸酯-13-乙酸酯不会激活这些因子,并且HepG2细胞中似乎需要从头合成蛋白质才能通过肿瘤坏死因子-α激活基因。