Page 51 - 《中国药科大学学报》2025年第5期

学报
Journal of China Pharmaceutical University 2025, 56(5): 583 − 591 583

NSUN2 通过介导 ARMC9 的 m C 5 修饰促进胃癌细胞的增殖、

转移和侵袭

李 越，陈 栋，王 瑾，彭 怡，张远琦，杨 芬 ，王学军 **
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（南京医科大学基础医学院, 南京 211166）

摘 要 为研究 NOP2/Sun RNA 甲基转移酶 2（NOP2/Sun RNA methyltransferase 2，NSUN2）对胃癌恶性进展的影响及其
潜在机制，使用 TCGA 数据库分析发现胃癌组织中 NSUN2 表达水平显著升高；Western blot 发现，与胃黏膜上皮细胞相比，
NSUN2 在胃癌细胞中表达上调；集落形成实验显示，NSUN2 过表达细胞中集落形成能力增高；Transwell 实验也证实
NSUN2 高表达时，发生迁移和侵袭的细胞数量显著增多。进一步通过数据库分析推测 ARMC 可能是 NSUN2 的下游靶分
子，接着通过 MeRIP-qPCR 揭示 NSUN2 高表达可以提高 ARMC9 的 m C 5 修饰水平，并且降低 ARMC9 mRNA 的降解速率，
从而提高其蛋白表达水平。此外，过表达 ARMC9 可以增强细胞的集落形成能力和迁移侵袭能力。上述结果显示，
NSUN2 可以通过提高 ARMC9 mRNA 的 m C 5 修饰水平，提高其稳定性，增强其表达，从而促进胃癌进展，因此 NSUN2 和
ARMC9 可以作为胃癌进展的潜在治疗靶标。
关键词 5-甲基胞嘧啶；甲基转移酶；NOP2/Sun RNA 甲基转移酶 2；犰狳重复序列 9；胃癌；肿瘤标志物
中图分类号 R965；Q279 文献标志码 A 文章编号 1000−5048(2025)05−0583−09
doi：10.11665/j.issn.1000−5048.2025031101

引用本文 李越，陈栋，王瑾，等. NSUN2 通过介导 ARMC9 的 m C 5 修饰促进胃癌细胞的增殖、转移和侵袭 [J]. 中国药科大学学报，2025，
56（5）：583 − 591.

Cite this article as: LI Yue, CHEN Dong, WANG Jin, et al. NSUN2 promotes proliferation, migration, and invasion of gastric cancer cells by
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mediating m C modification of ARMC9[J]. J China Pharm Univ, 2025, 56(5): 583 − 591.

NSUN2 promotes proliferation, migration, and invasion of gastric cancer cells
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by mediating m C modification of ARMC9
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LI Yue, CHEN Dong, WANG Jin, PENG Yi, ZHANG Yuanqi, YANG Fen , WANG Xuejun **
School of Basic Medical Science, Nanjing Medical University, Nanjing 211166, China

Abstract To investigate the impact and underlying mechanism of NOP2/Sun RNA methyltransferase 2
(NSUN2) on gastric cancer progression, TCGA database was used and revealed a significant upregulation of
NSUN2 expression in gastric cancer tissues. Western blot analysis revealed that NSUN2 was upregulated in
gastric cancer cells compared with gastric mucosal epithelial cells. Colony formation assays demonstrated an
enhanced colony-forming capacity in NSUN2-overexpressing cells. Furthermore, Transwell assays showed a
marked increase in cell migration and invasion upon high NSUN2 expression. Moreover, TCGA database
analysis suggested ARMC9 as a potential downstream target of NSUN2. Subsequently, MeRIP-qPCR analysis
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revealed that NSUN2 overexpression could increase m C modification of ARMC9 mRNA, and reduce its
degradation rate, thus enhancing protein expression. Additionally, ARMC9 overexpression augmented cellular
colony formation and migratory and invasive capabilities. These findings indicate that NSUN2 promotes gastric
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cancer progression by elevating m C modification of ARMC9 mRNA, increasing its stability and enhancing its
expression, therefore, NSUN2 and ARMC9 may serve as potential therapeutic targets for gastric cancer.

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收稿日期 2025-03-11 通信作者 Tel：025-86869322 E-mail：yangfen@njmu.edu.cn
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Tel：025-86869322 E-mail：wangxuejun@njmu.edu.cn
基金项目 国家自然科学基金项目（No. 32270649）