Yu Zhefei, Yang Yang
The First Affiliated Hospital of Guangxi University Of Chinese Medicine, Nanning, Guangxi, China.
Front Oncol. 2024 Nov 29;14:1483435. doi: 10.3389/fonc.2024.1483435. eCollection 2024.
Gastric cancer (GC) is one of the leading causes of cancer-related death worldwide. N6-methyladenosine (m6A) modification is the most prominent epigenetic modification of eukaryotic mRNAs, and methyltransferase-like 3 (METTL3), a core component of the methyltransferase complex, catalyzes m6A modification. The results of previous studies indicate that the expression level of METTL3 is significantly elevated in gastric cancer tissues and cells. In addition, fluctuations in m6A levels induced by METTL3 are closely associated with the malignant progression of tumors as well as the poor prognosis of patients with gastric cancer. In this review, we focus on the potential mechanism of METTL3 in gastric cancer, and through our analysis, we suggest that targeting METTL3 could be a new therapeutic tool for treating GC.
胃癌(GC)是全球癌症相关死亡的主要原因之一。N6-甲基腺苷(m6A)修饰是真核生物mRNA最显著的表观遗传修饰,甲基转移酶样3(METTL3)作为甲基转移酶复合物的核心成分,催化m6A修饰。先前的研究结果表明,METTL3在胃癌组织和细胞中的表达水平显著升高。此外,METTL3诱导的m6A水平波动与肿瘤的恶性进展以及胃癌患者的不良预后密切相关。在本综述中,我们聚焦于METTL3在胃癌中的潜在机制,通过分析,我们认为靶向METTL3可能是治疗GC的一种新的治疗手段。