在我们的前期研究中，对125对胃癌配对组织进行外显子测序研究，构建了基因突变图谱。通过分析基因突变与预后的关系发现，包括粘蛋白17（Mucin17，MUC17）在内的57.0%的突变基因与病人的预后较好相关。在本课题中，我们以突变频率较高的MUC17为研究对象，阐明携带突变型MUC17的患者预后相对较好的分子机制。我们的结果表明：突变型MUC17在胃癌组织中的表达显著增加，且与炎症因子的表达正相关；突变型MUC17通过其保守的EGF样结构域发挥其抑制胃癌细胞增殖及抗炎的功能；这一发现提示突变型MUC17的作用可能与机体适应环境暴露密切相关。为此，我们将对突变型MUC17在胃癌中的生物学作用和分子调控机制进行深入探讨，为胃癌的诊治，甚至为基因突变和肿瘤的关系研究提供新的思路和科学依据。

In our previous study, we constructed mutational landscape of gastric cancer by exomic sequencing 125 gastric cancer tissues and matched normal tissues. Through survival analysis, we found that 57.0% mutant genes (including Mucin17，MUC17 ) were associated with well prognosis. In this study, we study the function of mutant MUC17 to explore the mechanism that patients carried mutant MUC17 had a better prognosis. Our result showed that the expression of Mutant type was higher than wild type MUC17 and the expression of mutant type MUC17 was associated with inflammation factor. Mutant MUC17 inhibits gastric cancer cell proliferation and defenses inflammation through its constant EGF domain. That might be the mechanism that mutant MUC17 benefits patients’ survive. In this study, we will explore the function and mechanism of mutant MUC17, these results will offer the new strategy for gastric cancer study and relation between gene mutation and cancer.