Helicobacter pylori (H. pylori) is implicated in the aberrant proliferation and malignant transformation of gastric mucosal cells, heightening the risk of gastric cancer (GC). HN1 is involved in the development of various tumors. However, precise mechanistic underpinnings of HN1 promoting GC progression in H. pylori remain elusive. The study collected 79 tissue samples of GC patients, including 47 with H. pylori-positive GC and 32 H. pylori-negative controls. Using human gastric epithelial cells (GES-1) and human gastric adenocarcinoma cells (HGC-27), the effect of overexpression / knocking down of HN1 and H. pylori infection was evaluated on cell function (proliferation, migration, apoptosis), cytoskeleton, and expression of cell malignant phenotype factors that promote the malignant biological behavior of cancer cells. The expression of HN1 in GC tissues is higher than that in paracancerous tissue and is closely related to infiltration, lymphatic metastasis, distant metastasis, survival, and H. pylori infection. Downregulation of HN1 effectively hinders the ability of H. pylori strains 26695 and SS1 to promote migration of GES-1 and HGC-27 cells, while lowering the expression of key indicators associated with malignant phenotype. Downregulated GSK3B, β-catenin, and Vimentin after knockdown Integrinβ1, but HN1 expression remained largely unchanged, when HN1 and Integrinβ1 were knocked down, GSK3B, β-catenin, and Vimentin expression were considerably reduced. Our research demonstrated the crucial role of HN1 in H. pylori-induced acquisition of a malignant phenotype in GES-1 cells. Knockdown of HN1 blocked the pathogenic mechanism of H. pylori-induced GC and downregulated the expression of GSK3Β, β-catenin and Vimentin via Integrin β1.

幽门螺杆菌（H. pylori）与胃粘膜细胞的异常增殖和恶性转化有关，从而增加患胃癌（GC）的风险。 HN1参与多种肿瘤的发生发展。然而，HN1 促进幽门螺杆菌GC 进展的精确机制基础仍然难以捉摸。该研究收集了 79 份 GC 患者的组织样本，其中包括 47 份幽门螺杆菌阳性 GC 和 32 份幽门螺杆菌阴性对照。使用人胃上皮细胞（GES-1）和人胃腺癌细胞（HGC-27），评估过表达/敲低HN1和幽门螺杆菌感染对细胞功能（增殖、迁移、凋亡）、细胞骨架、以及促进癌细胞恶性生物学行为的细胞恶性表型因子的表达。 HN1在GC组织中的表达高于癌旁组织，与浸润、淋巴转移、远处转移、生存及H. pylori感染密切相关。 HN1的下调有效阻碍了幽门螺杆菌菌株26695和SS1促进GES-1和HGC-27细胞迁移的能力，同时降低了与恶性表型相关的关键指标的表达。敲低Integrinβ1后GSK3B、β-catenin和Vimentin表达下调，但HN1表达基本保持不变，当敲低HN1和Integrinβ1时，GSK3B、β-catenin和Vimentin表达显着降低。我们的研究证明了 HN1 在幽门螺杆菌诱导的 GES-1 细胞恶性表型获得中的关键作用。 HN1 的敲低阻断了幽门螺杆菌诱导的 GC的致病机制，并通过整合素 β1 下调了 GSK3β、β-catenin 和 Vimentin 的表达。