EHF 作为介导细胞迁移的关键调节因子，可能促进人子宫内膜癌的肿瘤免疫浸润和进展

Public databases were utilized to investigate the molecular features of EHF and its significance in the pathogenesis of EC. Analyses including single - gene correlation, functional enrichment, and immune infiltration were conducted. We used lentiviral-mediated EHF silencing in HEC-1B cells to examine EHF's impact on cell cycle, immigration, invasion, and proliferation.

High EHF expression was linked to a more dismal prognosis of EC. The degree of tumor invasion, histologic type and stage, and clinical stage were significantly associated with EHF overexpression. Functional enrichment research conclusively indicated that EHF was closely linked to various activities, including the cell cycle, metabolic pathways, and interleukin 17 signaling pathway. The expression of EHF exhibited a negative connection with the presence of dendritic cells, natural killer (NK) cells, CD4 + type 1 T-helper cells, and the varying infiltration levels of other immune cells. In vitro study revealed increased EHF levels in endothelial cell tissues and cell lines. Analyses of functional components showed that EHF greatly enhances EC cell migration and development.

Elevated EHF expression in EC patients correlated with diminished immune cell infiltration and a worse outcome. Decreasing EHF levels also affected the invasion and proliferation of EC cells. These findings highlight EHF as a putative prognostic and diagnostic biomarker for EC.