研究表明PGD2/PTGDR2信号抑制肿瘤的发生发展，然而PGD2/PTGDR2信号对胃癌及胃癌干细胞（GCSC）的作用及机制尚不清楚，我们发现PGD2/PTGDR2信号通路蛋白（PGD2合成酶PTGDS及其受体PTGDR2）在胃癌组织中显著低表达且与胃癌患者的预后相关，它们在胃癌组织中的表达与GCSC标记分子（Sall4、Lgr5等）呈显著负相关，体外实验亦发现PGD2/PTGDR2信号促进胃癌细胞的自噬性死亡并抑制GCSC的干细胞特性，以上结果说明PGD2/PTGDR2信号具备调控GCSC恶性生物学功能的潜力。本研究将采用Crispr/cas9基因编辑、免疫共沉淀等多种细胞与分子生物学技术，结合PTGDR2基因敲除动物模型探讨PGD2/PTGDR2信号对胃癌干细胞自噬的影响及其在胃癌干细胞调控中的作用机制。本课题的完成将揭示调控胃癌干细胞功能的新机制，为胃癌诊疗提供新的思路和方法。

Previous studies have shown that PGD2/PTGDR2 signal inhibited the tumorigenesis and progression of cancer. However, the role and mechanism of PGD2/PTGDR2 signal in gastric cancer and gastric cancer stem cells is unclear. We found that the expression of PGD2/PTGDR2 signaling-related proteins (PGD2 synthase PTGDS and its receptor PTGDR2) in gastric cancer tissues were significantly lower than adjacent tissue and was associated with prognosis of patients. The expression of PTGDS and PTGDR2 was significantly negatively correlated with gastric cancer stem cell marker molecules (Sall4, Lgr5, etc.). In vitro experiments also showed that PGD2/PTGDR2 signal induced autophagic-death and inhibited stemness of GCSC. In this study, we will investigate the action of PGD2/PTGDR2 signal in autophagy and its mechanism by using Crispr/cas9 gene editing, immunoprecipitation, other cell and molecular biology techniques and PTGDR2 knockout animal model. The completion of this study will explain the new mechanism of GCSCs and provide new ideas and methods for the diagnosis and treatment of gastric cancer.