Abstract：
Epstein-Barr virus (EBV) infection has a strong correlation with the development of nasopharyngeal carcinoma (NPC). Aquaporin 3 (AQP3), a member of the aquaporin family, plays an important role in tumor development, especially in epithelial-mesenchymal transition. In this study, the expression of AQP3 in EBV-positive NPC cells was significantly lower than that in EBV-negative NPC cells. Western blot and qRT-PCR analysis showed that LMP1 down-regulated the expression of AQP3 by activating the ERK pathway. Cell biology experiments have confirmed that AQP3 affects the development of tumor by promoting cell migration and proliferation in NPC cells. In addition, AQP3 can promote the lysis of EBV in EBV-positive NPC cells. The inhibition of AQP3 expression by EBV through LMP1 may be one of the mechanisms by which EBV maintains latent infection-induced tumor progression.
摘要：
EB病毒(EBV)感染与鼻咽癌的发生发展密切相关。水通道蛋白3(AQP3),水通道蛋白家族的一员,在肿瘤的发展中起着重要的作用，尤其是在上皮-间质转化中。在这项研究中,EBV阳性NPC细胞中AQP3的表达明显低于EBV阴性NPC细胞。Westernblot和qRT-PCR分析表明，LMP1通过激活ERK通路下调AQP3的表达。细胞生物学实验证实AQP3在NPC细胞中通过促进细胞迁移和增殖来影响肿瘤的发展。此外,AQP3可以促进EBV在EBV阳性NPC细胞中的溶解。EBV通过LMP1抑制AQP3表达可能是EBV维持潜伏感染诱导的肿瘤进展的机制之一。
