ULK1 (Unc-51-like kinase 1) is an evolutionarily conserved serine/threonine kinase that plays a central role in the regulation of autophagy. ULK1 is associated with prognosis for metastasis and survival in several tumors. However, its relationship with Epstein-Barr virus (EBV) has not been studied. We found that the expression of ULK1 in EBV-associated gastric cancer cells was lower than that in EBV-negative gastric cancer cells. Further, a luciferase reporter gene assay showed that miR-BART2-3p directly targets ULK1. EBV-miR-BART2-3p attenuated endogenous protein expression levels of some autophagy-related genes. MiR-BART2-3p could thus be involved in the regulation of autophagy. Most important, our research indicates that miR-BART2-3p targets ULK1, resulting in downregulation of epithelial-mesenchymal transformation (EMT) -associated marker proteins and reducing EMT and cell migration. Our study shows that modulation of ULK1 is the likely mechanism by which miR-BART2-3p participates in the regulation of autophagy and cancer cell migration.

ULK1（Unc-51 样激酶 1）是一种进化上保守的丝氨酸/苏氨酸激酶，在自噬调节中起核心作用。ULK1 与几种肿瘤的转移和生存预后相关。然而，尚未研究其与 Epstein-Barr 病毒 (EBV) 的关系。我们发现 ULK1 在 EBV 相关胃癌细胞中的表达低于 EBV 阴性胃癌细胞。此外，荧光素酶报告基因分析显示 miR-BART2-3p 直接靶向 ULK1。EBV-miR-BART2-3p 减弱了一些自噬相关基因的内源蛋白表达水平。因此，MiR-BART2-3p 可能参与自噬的调节。最重要的是，我们的研究表明 miR-BART2-3p 靶向 ULK1，导致上皮间质转化 (EMT) 相关标记蛋白的下调并减少 EMT 和细胞迁移。我们的研究表明，ULK1 的调节是 miR-BART2-3p 参与调节自噬和癌细胞迁移的可能机制。