Gastric cancer (GC) is one of the most common malignant cancers in the world. c-Myc, a well-known oncogene, is commonly amplified in many cancers, including gastric cancer. However, it is still not completely understood how c-Myc functions in GC. Here, we generated a stomach-specific c-Myc transgenic mouse model to investigate its role in GC. We found that overexpression of c-Myc in Atp4b+ gastric parietal cells could induce gastric adenoma in mice. Mechanistically, c-Myc promoted tumorigenesis via the AKT/mTOR pathway. Furthermore, AKT inhibitor (MK-2206) or mTOR inhibitor (Rapamycin) inhibited the proliferation of c-Myc overexpressing gastric cancer cell lines. Thus, our findings highlight that gastric tumorigenesis can be induced by c-Myc overexpression through activation of the AKT/mTOR pathway.

中文翻译：

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胃特异性 c-Myc 过表达通过 AKT/mTOR 信号驱动小鼠胃腺瘤。

胃癌（GC）是世界上最常见的恶性肿瘤之一。c-Myc 是一种众所周知的致癌基因，通常在包括胃癌在内的许多癌症中被扩增。然而，仍然没有完全理解 c-Myc 在 GC 中的作用。在这里，我们生成了胃特异性 c-Myc 转基因小鼠模型来研究其在 GC 中的作用。我们发现 c-Myc 在 Atp4b+ 胃壁细胞中的过表达可以诱导小鼠胃腺瘤。从机制上讲，c-Myc 通过 AKT/mTOR 通路促进肿瘤发生。此外，AKT 抑制剂（MK-2206）或 mTOR 抑制剂（雷帕霉素）抑制过表达 c-Myc 的胃癌细胞系的增殖。因此，我们的研究结果强调，通过激活 AKT/mTOR 通路，c-Myc 过表达可以诱导胃肿瘤发生。