前列腺素D2（PGD2）已被证明可以限制多种癌症的发生和发展，然而其潜在的分子机制尚未完全阐明。本研究调查了PGD2对富集的胃癌干细胞（GCSCs）的生物功能以及其潜在的分子机制，为胃癌（GC）治疗提供了理论基础和潜在治疗药物。通过酶联免疫吸附测定法（ELISA）检测血浆中的PGD2水平。在SGC-7901和HGC-27细胞系中沉默脂类过氧化物酶原D合成酶（L-PTGDS）和前列腺素D2受体2（PTGDR2）的表达。利用细胞计数试剂盒-8、Transwell、流式细胞术和免疫印迹分析，确定GCSCs的细胞存活率、侵袭能力、凋亡和干细胞特性。采用体内异种移植模型评估肿瘤生长。临床上发现，GC患者血浆中的PGD2水平显著降低。PGD2抑制了GCSCs的存活、侵袭和干细胞特性，并增加了其凋亡。L-PTGDS和PTGDR2的下调促进了GCSCs的存活、侵袭和干细胞特性，并减少了其凋亡。此外，通过下调PTGDR2的表达，PGD2对GCSCs的抑制作用消除。体内实验的结果与体外实验一致。我们的数据表明，PGD2可能是GC临床管理中的重要标志物和潜在治疗靶点。L-PTGDS/PTGDR2可能是GC治疗的关键靶点之一。PGD2/PTGDR2信号影响了GCSCs的存活、侵袭、凋亡和干细胞特性，并预防了GC的进展。 版权所有© Bentham Science Publishers; 如有任何疑问，请发送电子邮件至epub@benthamscience.net。

Prostaglandin D2 (PGD2) has been shown to restrict the occurrence and development of multiple cancers; nevertheless, its underlying molecular mechanism has not been fully elucidated. The present study investigated the effect of PGD2 on the biological function of the enriched gastric cancer stem cells (GCSCs), as well as its underlying molecular mechanism, to provide a theoretical basis and potential therapeutic drugs for gastric cancer (GC) treatment.The plasma PGD2 levels were detected by Enzyme-linked immunosorbent assay (ELISA). Silencing of lipocalin prostaglandin D synthetases (L-PTGDS) and prostaglandin D2 receptor 2 (PTGDR2) was carried out in GCSCs from SGC-7901 and HGC-27 cell lines. Cell Counting Kit-8, transwell, flow cytometry, and western blotting assays were used to determine cell viability, invasion, apoptosis, and stemness of GCSCs. In vivo xenograft models were used to assess tumor growth.Clinically, it was found that the plasma PGD2 level decreased significantly in patients with GC. PGD2 suppressed viability, invasion, and stemness and increased the apoptosis of GCSCs. Downregulating L-PTGDS and PTGDR2 promoted viability, invasion, and stemness and reduced the apoptosis of GCSCs. Moreover, the inhibition of GCSCs induced by PGD2 was eliminated by downregulating the expression of PTGDR2. The results of in vivo experiments were consistent with those of in vitro experiments.Our data suggest that PGD2 may be an important marker and potential therapeutic target in the clinical management of GC. L-PTGDS/PTGDR2 may be one of the critical targets for GC therapy. The PGD2/PTGDR2 signal affects the viability, invasion, apoptosis, and stemness of GCSCs and prevents the progression of GC.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.