Gastric cancer (GC) is a heterogeneous disease whose development is accompanied by alterations in a variety of pathogenic genes. The phospholipase C Delta 3 enzyme is a member of the phospholipase C family, which controls substance transport between cells in the body. However, its role in gastric cancer has not been discovered. The purpose of this study was to investigate the expression and mechanism of action of PLCD3 in connection to gastric cancer. By Western blot analysis and immunohistochemistry, PLCD3 mRNA and protein expression levels were measured, with high PLCD3 expression suggesting poor prognosis. In N87 and HGC-27 cells, the silencing of PLCD3 using small interfering RNA effectively induced apoptosis and inhibited tumor cell proliferation, invasion, and migration. Conversely, overexpression of PLCD3 using overexpressed plasmids inhibited apoptosis in AGS and BGC-823 cells and promoted proliferation, migration, and invasion. In order to investigate the underlying mechanisms, we conducted further analysis of PLCD3, which indicates that this protein is closely related to the cell cycle and EMT. Additionally, we found that overexpression of PLCD3 inhibits apoptosis and promotes the development of GC cells through JAK2/STAT3 signaling. In conclusion, PLCD3 inhibits apoptosis and promotes proliferation, invasion, and migration, which indicated that PLCD3 might serve as a therapeutic target for gastric cancer.

胃癌（GC）是一种异质性疾病，其发展伴随着多种致病基因的改变。磷脂酶 C Delta 3 酶是磷脂酶 C 家族的成员，控制体内细胞之间的物质运输。然而，其在胃癌中的作用尚未被发现。本研究的目的是探讨PLCD3在胃癌中的表达及其作用机制。通过Western blot分析和免疫组织化学检测PLCD3 mRNA和蛋白表达水平，PLCD3高表达提示预后不良。在N87和HGC-27细胞中，使用小干扰RNA沉默PLCD3可有效诱导细胞凋亡并抑制肿瘤细胞增殖、侵袭和迁移。相反，使用过表达质粒过表达 PLCD3 会抑制 AGS 和 BGC-823 细胞的凋亡，并促进增殖、迁移和侵袭。为了探究其潜在机制，我们对PLCD3进行了进一步分析，表明该蛋白与细胞周期和EMT密切相关。此外，我们发现 PLCD3 的过度表达可通过 JAK2/STAT3 信号传导抑制细胞凋亡并促进 GC 细胞的发育。总之，PLCD3抑制细胞凋亡并促进增殖、侵袭和迁移，这表明PLCD3可能作为胃癌的治疗靶点。