EFNB1 drives glioma progression and shapes the immune microenvironment: a potential prognostic biomarker

EFNB1驱动胶质瘤进展并塑造免疫微环境:一种潜在的预后生物标志物

阅读:2

Abstract

Gliomas, a heterogeneous group of tumors affecting the brain and spinal cord, present a significant clinical challenge. Ephrin B1 (EFNB1) has been implicated in various malignancies. However, its role in gliomas remained poorly understood. Hence, this study aimed to elucidate the connection between EFNB1 and the progression of glioma. A retrospective RNA-seq analysis was conducted by utilizing the data from glioma patients in the TCGA and CGGA databases. Kaplan-Meier survival analysis and multivariate regression models were employed to evaluate the prognostic significance of EFNB1. RT-PCR was used to quantify EFNB1 expression in glioma tissues and cell lines. Meanwhile, in vitro assays were carried out to assess its functional roles in glioma cells. Our findings demonstrated that EFNB1 expression was significantly elevated in gliomas and other cancers. Moreover, high EFNB1 expression was closely correlated with advanced clinical stages and poor prognosis. Notably, multivariate analysis identified EFNB1 as an independent prognostic factor for overall survival. KEGG pathway analysis suggested that EFNB1 was involved in critical biological processes, including the cell cycle, protein processing in the endoplasmic reticulum, Epstein-Barr virus infection, and Salmonella infection. Furthermore, EFNB1 expression was associated with immune cell infiltration, particularly Th2 cells, macrophages, and plasmacytoid dendritic cells. In glioma cells, EFNB1 expression was markedly increased. Consequently, functional experiments demonstrated that EFNB1 knockdown inhibited glioma cell proliferation, invasion, and migration. These results highlighted EFNB1 as a novel independent prognostic biomarker and suggest its potential role in shaping the immunological microenvironment of gliomas.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。