能量代谢异常是肿瘤细胞的重要特征之一。肿瘤细胞可通过激活脂肪酸β氧化，为细胞转移提供充足的能量。前期工作中，我们发现鼻咽癌存在脂肪堆积现象；同时发现具有促进鼻咽癌细胞转移的EB病毒编码潜伏膜蛋白LMP2A可增加胞内脂肪堆积，并与AMPK磷酸化和脂肪酸β氧化的关键酶肉毒棕榈酰转移酶（carnitine palmitoyltransferase-1C，CPT1C）的表达上调有关。因此，我们提出科学假设：LMP2A通过AMPK通路调控宿主细胞中CPT1C的表达，促进胞内脂肪酸β氧化，从而为鼻咽癌的转移行为提供能量。本研究拟进一步证实LMP2A对鼻咽癌中CPT1C的调控机制，探索CPT1C对鼻咽癌脂肪酸代谢的影响，并阐明EB病毒通过调控鼻咽癌细胞脂肪酸代谢促进转移行为的分子机理。通过上述研究，从脂肪酸代谢异常的角度探讨EB病毒感染在鼻咽癌发生发展中的作用及其分子机制，为鼻咽癌能量代谢靶向性治疗提供

Deregulating cellular energetics is one of the hallmarks of cancer. Tumor cells generate sufficient energy to enhance the metastatic capability by activating the fatty acid beta-oxidation. In previous study, we found that lipid droplets (LDs) accumulate in nasopharyngeal carcinoma (NPC). Epstein-Barr virus (EBV) encoded latent membrane protein (LMP2A) has been confirmed to promote NPC metastasis. We found that the expression of LMP2A in NPC cells increases intracellular LDs, activates AMP-activated protein kinase (AMPK), and stabilizes the expression of carnitine palmitoyltransferase-1C (CPT1C), an enzyme responsible for fatty acid beta-oxidation. Thus, we hypothesize that LMP2A would promote NPC cell metastasis by activating the cellular fatty acid beta-oxidation via AMPK/CPT1C axis. In this study, we aim to further study the mechanism of LMP2A in modulating the expression of CPT1C and investigate the effect of CPT1C on fatty acid metabolism, in order to explore the function of fatty acid metabolism reprogrammed by EBV in NPC metastasis. With this study, we will better understand the role of EBV in the pathogenesis of NPC, thereby providing theoretic foundation for targeting energy metabolism in NPC treatment.