Salvador homologue 1 (SAV1), which is reported to act as a tumor suppressor in different types of cancer, is one of the key components of the Hippo pathway. However, the expression and mechanisms of SAV1 in the development and progression of gastric cancer (GC) remain to be elucidated. Immunohistochemistry (IHC) was performed in the present study to assess the expression levels of SAV1 and lysine-specific demethylase 2B (KDM2B) in GC tissues. The biological effects of SAV1 on GC cell proliferation, migration, and invasion were studied in vitro. KDM2B transcriptionally regulates SAV1 expression in several GC cell lines, and molecular experiments were performed to investigate underlying mechanisms. The expression level of SAV1 was significantly decreased in GC tissues and cell lines, negatively associated with tumor invasion depth, lymph node metastasis, and TNM stage, and positively associated with the overall survival of patients with GC. SAV1 overexpression inhibited the proliferation, migration, and invasion of GC cells. Further mechanistic studies revealed that KDM2B transcriptionally regulated SAV1 expression and further regulated the Hippo signaling pathway. To conclude, the present study demonstrated that KDM2B transcriptionally regulated SAV1 expression and promoted GC progression.

据报道，萨尔瓦多同源物 1 (SAV1) 在不同类型的癌症中充当肿瘤抑制因子，是 Hippo 通路的关键组成部分之一。然而，SAV1在胃癌（GC）发生和进展中的表达和机制仍有待阐明。本研究采用免疫组织化学 (IHC) 来评估 GC 组织中 SAV1 和赖氨酸特异性去甲基酶 2B (KDM2B) 的表达水平。体外研究了SAV1对GC细胞增殖、迁移和侵袭的生物学效应。KDM2B 在几种 GC 细胞系中转录调节 SAV1 表达，并进行分子实验来研究潜在机制。SAV1的表达水平在GC组织和细胞系中显着降低，与肿瘤浸润深度、淋巴结转移和TNM分期呈负相关，与GC患者的总生存期呈正相关。SAV1过表达抑制GC细胞的增殖、迁移和侵袭。进一步的机制研究表明，KDM2B 转录调节 SAV1 表达，并进一步调节 Hippo 信号通路。总之，本研究证明 KDM2B 转录调节 SAV1 表达并促进 GC 进展。