| Gastric cancer is one of the most common malignant cancers.China is an area with high incidence of gastric cancer.Since early gastric cancer usually lasts for a long time and lacks obvious symptoms,patients with gastric cancer are often diagnosed as advanced gastric cancer,with poor prognosis and low survival rate.During the progression of gastric cancer,the role of genetic factors can not be ignored.SETD2 is currently the only reported trimethyltransferase of H3K36,which is closely related to the progression of many cancers.Setd2 is also commonly mutated in gastric cancer,which affects the occurrence and development of tumor.However,it is not clear how SETD2 affects the progression of gastric cancer.c-Myc,an oncogene,is abnormally highly expressed in a variety of tumors,including gastric cancer.Hi-Myc mouse model with high expression of c-myc has been widely used in prostate cancer research,but there is no gastric cancer mouse model with high expression of c-Myc at present,and it is unclear how c-Myc functions in gastric cancer.Hence,in this study,we successfully constructed c-Myc knock-in gastric cancer mouse model driven by Atp4b-cre recombinase on the one hand,and found that the gastric cancer caused by c-Myc has the characteristics of early intestinal type gastric cancer,and may be induced by activating AKT/m TOR pathway through tissue section staining and transcriptome next generation sequencing.On the other hand,based on c-Myc mouse model of gastric cancer,Setd2 knockout mouse model of gastric cancer was constructed.It was found that the deletion of Setd2 would advance the development of tumor.In this study,we first established a c-Myc and Setd2 gene modified gastric cancer mouse model,which provided a brand-new animal model for subsequent gastric cancer research.Meanwhile,it is of important clinical significance for the diagnosis and molecular targeted treatment of early gastric cancer. |
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