Abstract
Globally, gastric cancer (GC) is an urgent health concern, necessitating an understanding of its genetic and epigenetic regulation. The tumor suppressor Setd2, H3K36me3 methyltransferase, has been associated with malignancies. The underlying signaling mechanisms and the function of Setd2 in GC aggravation are yet unclear. To figure out this question, we utilized a mouse model with c-Myc overexpression and Setd2 knockout in gastric parietal cells to conduct histological and molecular analysis. Our results demonstrated that deletion of Setd2 exacerbated gastric adenoma induced by c-Myc overexpression. Moreover, we revealed that PI3K/AKT signaling pathway contributed to the development of gastric adenoma, offering GC patients a potentially effective treatment approach.