Liu Jun-Ping, Cassar Lucy, Pinto Alex, Li He
Department of Immunology, Central Eastern Clinical School, Monash University, AMREP, Commercial Road, Prahran, Melbourne, Victoria 3181, Australia.
Cell Res. 2006 Oct;16(10):809-17. doi: 10.1038/sj.cr.7310098.
Nasopharyngeal carcinoma (NPC) is a common cancer in Southern China and Southeast Asia. The disease is a poorly differentiated carcinoma without effective cure, and the mechanism underlying its development remains largely unknown. Of several factors identified in NPC aetiology in recent years, Epstein-Barr virus (EBV) infection has emerged to be most important. In almost all NPC cells, EBV uses several intracellular mechanisms to cause oncogenic evolution of the infected cells. One such mechanism by which EBV infection induces cellular immortalization is believed to be through the activation of telomerase, an enzyme that is normally repressed but becomes activated during cancer development. Studies show that greater than 85% of primary NPC display high telomerase activity by mechanisms involving EBV infection, consistent with the notion that EBV is commonly involved in inducing cell immortalization. More recently, different EBV proteins have been shown to activate or inhibit the human telomerase reverse transcriptase gene, by modulating intracellular signalling pathways. These findings suggest a new model with a number of challenges towards our understanding, molecular targeting and therapeutic intervention in NPC.
鼻咽癌（NPC）是中国南方和东南亚地区常见的癌症。这种疾病是一种低分化癌，没有有效的治愈方法，其发病机制在很大程度上仍然未知。在近年来确定的鼻咽癌病因的几个因素中，爱泼斯坦-巴尔病毒（EBV）感染已成为最重要的因素。在几乎所有的NPC细胞中，EBV利用多种细胞内机制导致受感染细胞发生致癌演变。EBV感染诱导细胞永生化的一种机制被认为是通过激活端粒酶，端粒酶是一种通常被抑制但在癌症发展过程中被激活的酶。研究表明，超过85%的原发性鼻咽癌通过涉及EBV感染的机制表现出高端粒酶活性，这与EBV通常参与诱导细胞永生化的观点一致。最近，不同的EBV蛋白已被证明通过调节细胞内信号通路来激活或抑制人类端粒酶逆转录酶基因。这些发现提示了一个新的模型，对我们理解、分子靶向和治疗鼻咽癌具有诸多挑战。
