Epstein-Barr virus-associated gastric carcinoma (EBVaGC) is characterized by the clonal growth of EBV-infected stomach epithelial cells. It has been reported that N⁶-methyladenosine (m⁶A) methylation can regulate the splicing, expression, decay and translation of mRNAs. Wilms' tumor 1-associating protein (WTAP) is an m⁶A “writer” with methyltransferase activity. An m⁶A RNA methylation quantification kit and immunofluorescence (IF) showed that the m⁶A total RNA methylation level of the Epstein-Barr virus-negative gastric carcinoma (EBVnGC) cell line (SGC7901) was higher than that in the EBVaGC cell line (GT38). To investigate the underlying mechanism of the downregulated expression of m⁶A RNA methylation, we analyzed the expression of WTAP. The results showed that the expression of WTAP protein in EBVaGC cell lines was significantly lower than that in EBVnGC cell lines according to western blotting and IF. Through plasmid overexpression and RNA interference technology, we further found that EBV-encoded small RNA1 (EBER1) could downregulate WTAP expression by activating the NF-κB signaling pathway. In addition, WTAP could increase proliferation and inhibit migration in gastric carcinoma cell lines. In summary, EBER1 of EBV potentially regulated WTAP by affecting the NF-κB signaling pathway and WTAP further affected cell proliferation and migration.

Epstein-Barr 病毒相关胃癌 (EBVaGC) 的特征在于 EBV 感染的胃上皮细胞的克隆生长。据报道，N ⁶ -甲基腺苷（m ⁶ A）甲基化可以调节mRNA的剪接、表达、衰变和翻译。Wilms 的肿瘤 1 相关蛋白 (WTAP) 是一种具有甲基转移酶活性的 m ⁶ A“作家”。m ⁶ A RNA甲基化定量试剂盒和免疫荧光（IF）显示Epstein-Barr病毒阴性胃癌（EBVnGC）细胞系（SGC7901）的m ⁶ A总RNA甲基化水平高于EBVaGC细胞系。 (GT38)。探讨m ^{6表达下调的潜在机制}一个RNA甲基化，我们分析了WTAP的表达。结果表明WTAP蛋白在EBVaGC细胞系中的表达显着低于EBVnGC细胞系中的蛋白质印迹和IF。通过质粒过表达和RNA干扰技术，我们进一步发现EBV编码的小RNA1（EBER1）可以通过激活NF-κB信号通路来下调WTAP的表达。此外，WTAP 可以增加胃癌细胞系的增殖并抑制迁移。总之，EBV的EBER1可能通过影响NF-κB信号通路来调节WTAP，而WTAP进一步影响细胞增殖和迁移。