GCNT3 (core 2β-1,6-acetylglucosaminyltransferase) is a novel core mucin synthase. It is known that abnormal expression of GCNT3 promotes the progression of several human cancers. However, its relationship with Epstein-Barr virus (EBV) has not been comprehensively studied. We found GCNT3 expression in EBV-associated gastric cancer cells and tissues to be lower than in EBV-negative gastric cancer cells and tissues, and high expression was significantly associated with advanced tumor-lymph node metastasis. Luciferase reporter assay revealed that miR-BART1-5p directly targeted GCNT3. In addition, miR-BART1-5p mimics transfection was observed to reduce cell proliferation and migration, while miR-BART1-5p inhibitor increased cell proliferation and migration following transfection. In conclusion, both miR-BART1-5p and knockdown of GCNT3 inhibited cell proliferation and migration. In addition, EBV may regulate GCNT3 by affecting the NF-kB signaling pathway. E-cadherin, N-cadherin, vimentin, and p-ERK were found to be downstream molecules of the miR-BART1-5p/GCNT3 pathway.

中文翻译：

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MiR-BART1-5p靶向核心2β-1,6-乙酰基氨基葡萄糖氨基转移酶GCNT3，以抑制EBV相关胃癌中的细胞增殖和迁移。

GCNT3（核心2β-1,6-乙酰基氨基葡萄糖氨基转移酶）是一种新型核心粘蛋白合成酶。已知GCNT3的异常表达促进了几种人类癌症的进展。但是，其与爱泼斯坦-巴尔病毒（EBV）的关系尚未得到全面研究。我们发现与EBV相关的胃癌细胞和组织中的GCNT3表达低于在EBV阴性胃癌细胞和组织中的表达，而高表达与晚期肿瘤-淋巴结转移显着相关。萤光素酶报告基因检测显示miR-BART1-5p直接靶向GCNT3。另外，观察到miR-BART1-5p模拟转染减少细胞增殖和迁移，而miR-BART1-5p抑制剂增加转染后细胞增殖和迁移。综上所述，miR-BART1-5p和GCNT3的抑制均抑制细胞增殖和迁移。此外，EBV可能通过影响NF-kB信号传导途径来调节GCNT3。发现E-钙粘着蛋白，N-钙粘着蛋白，波形蛋白和p-ERK是miR-BART1-5p / GCNT3途径的下游分子。