Silins S L, Sculley T B
Bancroft Centre, Queensland Institute of Medical Research, Brisbane, Australia.
Int J Cancer. 1995 Jan 3;60(1):65-72. doi: 10.1002/ijc.2910600110.
Group I Epstein-Barr virus (EBV)-positive Burkitt's lymphoma (BL) cells display a surface phenotype characteristic of germinal centre B cells and readily undergo apoptosis in response to a variety of stimuli, including serum deprivation. Activation of EBV latent gene expression has been shown to increase the survival of these tumour cells by blocking programmed cell death. To investigate the nature of this protection, we assessed the function of the EBV latent EBNA-4 gene in a group I lymphoma line, dG75. Group I BL cells induced to undergo apoptosis in response to serum starvation were protected in the presence of EBNA-4 protein. A possible factor underlying this EBNA-4-associated survival was increased expression of the oncoprotein bcl-2, a known repressor of cell death. Together these data suggest that EBNA-4 plays an important role in the regulation of programmed cell death in BL tumour cells.
第一组爱泼斯坦-巴尔病毒（EBV）阳性的伯基特淋巴瘤（BL）细胞表现出生发中心B细胞的表面表型特征，并且在受到包括血清剥夺在内的多种刺激时容易发生凋亡。已证明EBV潜伏基因表达的激活可通过阻断程序性细胞死亡来提高这些肿瘤细胞的存活率。为了研究这种保护的本质，我们在第一组淋巴瘤细胞系dG75中评估了EBV潜伏EBNA-4基因的功能。在血清饥饿诱导下发生凋亡的第一组BL细胞在存在EBNA-4蛋白的情况下受到保护。这种与EBNA-4相关的存活的一个可能因素是癌蛋白bcl-2的表达增加，bcl-2是一种已知的细胞死亡抑制因子。这些数据共同表明，EBNA-4在BL肿瘤细胞程序性细胞死亡的调节中起重要作用。
