作为化学致癌物的代表项目，MNNG与胃癌（GC）的发病密切相关，其中N6-甲基腺苷（m6A）RNA甲基化被认为是关键的表观遗传事件。在我们之前的研究中，我们发现与体外对照细胞相比，甲基转移酶 METTL3 的 m6A 修饰在暴露于 MNNG 的恶性 GES-1 细胞（MC 细胞）中上调，并且长非编码 RNA SNHG7 作为 MNNG 暴露的恶性 GES-1 细胞（MC 细胞）的下游靶点。 METTL3。然而，METTL3 在 MNNG 诱导的 GC 中介导 SNHG7 轴的功能作用仍不清楚。在本研究中，我们不断研究 METTL3 在介导 MNNG 诱导的 GC 中 SNHG7 轴的功能作用。 RIP-PCR 和 m6A-IP-qPCR 用于检查 MNNG 诱导的 GC 中 METTL3/m6A/SNHG7 轴的分子机制。通过MNNG构建并暴露METTL3基因敲除小鼠模型。使用Western blot分析、IHC分析和RT-qPCR来测量METTL3、SNHG7和EMT标记物的表达。在本研究中，我们利用体外和体内模型证明，在 MNNG 诱导的 GC 肿瘤发生中，m6A 修饰调节因子 METTL3 通过 m6A/SNHG7 轴促进细胞 EMT 和生物学功能。总之，我们的研究为 MNNG 诱导的胃癌发生至关重要的关键表观遗传分子事件提供了新的见解。这些发现表明 METTL3 是 GC 治疗的潜在治疗靶点。

As a representative item of chemical carcinogen, MNNG is closely associated with the onset of gastric cancer (GC), where N6-methyladonosine (m6A) RNA methylation is recognized as a critical epigenetic event. In our previous study, we found that the m6A modification by methyltransferase METTL3 was up-regulated in MNNG-exposed malignant GES-1 cells (MC cells) compared to control cells in vitro, and long non-coding RNA SNHG7 as a downstream target of the METTL3. However, the functional role of METTL3 in mediating the SNHG7 axis in MNNG-induced GC remains unclear. In the present study, we continuously investigate the functional role of METTL3 in mediating the SNHG7 axis in MNNG-induced GC. RIP-PCR and m6A-IP-qPCR were used to examine the molecular mechanism underlying the METTL3/m6A/SNHG7 axis in MNNG-induced GC. A METTL3 knockout mice model was constructed and exposed by MNNG. Western blot analysis, IHC analysis, and RT-qPCR were used to measure the expression of METTL3, SNHG7, and EMT markers. In this study, we demonstrated that in MNNG-induced GC tumorigenesis, the m6A modification regulator METTL3 facilitates cellular EMT and biological functions through the m6A/SNHG7 axis using in vitro and in vivo models. In conclusion, our study provides novel insights into critical epigenetic molecular events vital to MNNG-induced gastric carcinogenesis. These findings suggest the potential therapeutic targets of METTL3 for GC treatment.